The development of targeted mAbs has transformed the treatment of moderate-to-severe asthma. The main clinical trial outcomes have focused on exacerbation reduction and lung function improvement. In the past few years, there have been many high-quality studies examining pathophysiologic effects of the biologic therapies, giving insight into their downstream impacts. Clinical remission is a growing area of interest, and many studies highlight the utility as well as the limitations of commonly available biomarkers to predict treatment response. This review synthesizes the results of recent clinical trials and related topics focusing on relevant updates to the literature since 2024, highlighting new indications for use, predictors of response, safety data, real-world comparative effectiveness, remission, and mechanistic advances.

The principles underlying asthma management are evolving from a reactive model focused on symptom relief and exacerbation management to a proactive approach to achieve full disease control, with consideration of on-treatment clinical remission and disease modification. The advent of biologic therapies targeting type 2 inflammation, and to an extent allergen immunotherapy, have shown promise in achieving a state of on-treatment remission. Emerging evidence suggests that biologics have the potential to induce remission and structural disease modification, but further studies are needed to assess these outcomes as the primary endpoint. To more accurately assess remission as a meaningful outcome in asthma, definitions need to be standardized and validated across studies with special consideration to incorporate biomarker changes and applicability to diverse populations, including children. Ultimately, the transition toward remission- or disease modification-based care may represent a new frontier in the care of asthma.

BACKGROUND:Transient increases in blood eosinophils may accompany dupilumab treatment, but these increases are rarely associated with clinical symptoms, and clinical significance in children needs further assessment. OBJECTIVE:We sought to evaluate long-term efficacy and safety of dupilumab in children 6 to 11 years old with type 2 asthma who completed the VOYAGE study and enrolled in the open-label extension study EXCURSION and experienced an early increase in blood eosinophils. METHODS:This post hoc analysis assessed annualized severe exacerbation rates, change from baseline in pre-bronchodilator percent predicted FEV1 and z score, 5-item Asthma Control Questionnaire-Interviewer Administered (ACQ-5-IA) score, fractional exhaled nitric oxide, blood eosinophils and total IgE, and safety in subgroups with early eosinophil increase (children with <500 cells/μL at baseline and ≥500 cells/μL at VOYAGE week 12). RESULTS:At VOYAGE week 12, 22.4% (35/156) had ≥500 eosinophils/μL. Dupilumab reduced exacerbation rates versus placebo during VOYAGE across subgroups, with effects maintained in EXCURSION. Children switching from placebo to dupilumab also experienced consistent improvements similar to children who had been receiving dupilumab. Improvements in percent predicted FEV1 and z score, questionnaire score, fractional exhaled nitric oxide, and total IgE were observed in children with and without early blood eosinophil increases. No safety differences were observed across subgroups. CONCLUSION:Dupilumab reduced exacerbations, improved lung function and asthma control, and decreased inflammatory biomarkers in children with type 2 asthma across subgroups with and without early blood eosinophil increases up to 2 years. No differences in dupilumab safety profile were observed in children with early eosinophil increases. CLINICAL TRIAL REGISTRATION:VOYAGE: ClinicalTrials.gov Identifier: NCT02948959; EXCURSION: ClinicalTrials.gov Identifier: NCT03560466.

Background:The Global Initiative for Asthma recommends patients with asthma uncontrolled on medium-dose inhaled corticosteroid (ICS) plus long-acting β2-agonist (LABA) therapy to first escalate their ICS dose before considering add-on biologic therapy despite acknowledging that high-dose ICS provides little additional benefit for most patients and carries an increased risk of adverse effects. Dupilumab, an IL-4Rα antagonist that inhibits signaling of IL-4 and IL-13, has demonstrated efficacy in patients with uncontrolled moderate-to-severe asthma and type 2 inflammation. Objective:The AIM4: Next Step study will evaluate whether earlier intervention with dupilumab provides clinical benefit compared to escalation to high-dose ICS/LABA. Methods:AIM4: Next Step (NCT06572228) is a randomized, double-blind, active-controlled study enrolling approximately 250 adolescents and adults with type 2 inflammatory asthma uncontrolled with medium-dose ICS/LABA treatment. Patients will be randomized 1:1 to receive dupilumab 300 mg every 2 weeks plus medium-dose ICS/LABA or placebo plus high-dose ICS/LABA. Results:The primary end point is the annualized rate of severe asthma exacerbations over 52 weeks. Key secondary end points include change from baseline in prebronchodilator forced expiratory volume in 1 second at week 12, annualized systemic corticosteroid exposure for exacerbations, and asthma control at week 12 based on 5-item Asthma Control Questionnaire. Conclusion:AIM4: Next Step is the first study designed to address an important gap in asthma management by directly comparing ICS dose escalation versus early biologic intervention with dupilumab in patients with uncontrolled type 2 inflammatory asthma. Findings may inform future treatment strategies for patients whose asthma remains uncontrolled despite ICS/LABA.

Network meta-analyses (NMAs) are an increasingly popular method in allergy, asthma, and immunology to inform comparative effectiveness among competing treatment options. They enable comparisons among treatments when no direct comparisons (ie, head-to-head randomized control trials) exist and strengthen inferences among direct comparisons by incorporating data from indirect comparisons. To inform optimal decision-making, allergy, asthma, and immunology clinicians, peer reviewers, journal editors, and policymakers must understand the fundamentals of how to assess NMA credibility. Through worked examples supporting American Academy of Allergy, Asthma & Immunology/American College of Allergy, Asthma and Immunology Task Force on Practice Parameters guidelines, we summarize the process of conducting an NMA and how to interpret results to inform clinical decision-making.

Randomized controlled trials underpin evidence-based medicine, but a growing proportion of trials contain implausible, inaccurate, or fabricated data. When such studies are incorporated into systematic reviews, they distort effect estimates, inflate evidence certainty, and can mislead the guideline recommendations that the reviews aim to inform. Within 8 recent American Academy of Allergy, Asthma & Immunology and American College of Allergy, Asthma and Immunology Joint Task Force on Practice Parameters (JTFPP) systematic reviews, 17% of trials published between 2021 and 2024 were problematic, and in a network meta-analysis of antihistamines for chronic urticaria, 39% of recent trials were excluded because of implausible data, statistical anomalies, and discrepancies between protocols and the final publication. The proliferation of generative artificial intelligence further facilitates the ability to produce superficially credible but flawed reports. Standardized tools have been developed to offer systematic approaches to detecting problematic trials, but robust safeguards such as verifiable ethics approval, prospective protocol registration, and adherence to structure reporting guidelines remain essential. As part of efforts to ensure quality research, the JTFPP will continue to update our systematic reviews to remove problematic trials as they are identified. We believe that this approach will promote the development of trustworthy guideline recommendations.

Background: Childhood-onset asthma is highly heritable, with nearly 200 risk loci identified in genome-wide association studies. Aggregated polygenic risk scores (PRSs) can be used to quantify genetic predisposition to asthma, but their power to predict asthma severity in multiancestral groups has not been previously evaluated. Objective: Our aim was to examine the predictive power of biobank-derived asthma PRSs in 4 multiancestry asthma study cohorts of children living in US urban environments. Methods: We generated PRSs for asthma, derived from a large-scale genome-wide association meta-analysis, and assessed genetic predictions across different subphenotypes of asthma and tested for associations between genetic asthma risk and measures of asthma severity. Results: PRS prediction was significantly stronger for more symptomatic asthma phenotypes (P < .001), and scores were significantly higher in difficult-to-control versus easy-to-control asthma (P = .02). Genetic risk was also significantly associated with more frequent exacerbations (P = .03), higher blood eosinophil levels (P = .01), and lower lung function (P < .001). Conclusion: Cumulative genetic risk for asthma is associated with disease severity and exacerbation risk in children with asthma.

Background: The nasal allergen challenge (NAC) is a tool for evaluating upper airway allergic responses. In the CRITICAL study, NAC with cockroach allergen was used to confirm clinical reactivity in sensitized individuals from urban environments before enrollment onto a subcutaneous immunotherapy trial. Objective: Immunologic and transcriptomic predictors of NAC responsiveness were identified. Methods: NAC was performed in 103 participants. Clinical responses were assessed by the Total Nasal Symptom Score (TNSS) and sneeze score (TSNEEZ), which scale positively with symptom severity. Baseline immunologic markers—including skin prick test wheal size, cockroach-specific IgE, IgG, and IgG4, and T-cell responses were evaluated. Nasal lavage samples were analyzed for gene expression modules. Clinical trial registration: ClinicalTrials.gov NCT03541187. Results: Larger skin prick test wheal sizes were significantly associated with positive NAC outcomes (2.2 mm larger than negative NAC) and lower reactive doses (hazard ratio = 1.10). Cockroach (i6 extract)-specific IgE levels were inversely correlated with TNSS, while levels of IgE, IgG, and IgG4 specific to the extract used for therapy showed no association. Higher IL-10 T-cell responses were observed in those without reaction, while Bla g 5 and Bla g 9 dominance correlated negatively with TNSS and positively with TSNEEZ, respectively. Transcriptomic analysis revealed that higher expression of eosinophil- and neutrophil-associated modules and lower expression of type 1 interferon, macrophage, and epithelial barrier modules were linked to positive NAC responses. Conclusion: NAC responsiveness to cockroach extract is influenced by skin test reactivity, T- and B-cell regulation, and nasal gene expression. These findings highlight the role of both adaptive and innate immunity in allergic airway responses and suggest potential biomarkers for clinical reactivity.

BACKGROUND:Escalating from medium-dose inhaled corticosteroid (ICS) to high-dose ICS in patients with asthma offers limited clinical benefit. OBJECTIVE:To assess the advantages of adding dupilumab to medium-dose ICS vs continuing high-dose ICS in patients with uncontrolled, moderate-to-severe asthma. METHODS:In the phase 3 QUEST study (NCT02414854), patients receiving medium- or high-dose ICS (>250-500 or >500 µg/d fluticasone propionate or equivalent) and long-acting β2-agonists (± third controller) initiated dupilumab 200/300 mg every 2 weeks or placebo for 52 weeks. This post hoc analysis of 1584 patients with baseline eosinophils of at least 150 cells/µL or fractional exhaled nitric oxide greater than or equal to 20 parts per billion and 1 or more exacerbations in the past year assessed annualized severe exacerbation rates, changes from baseline in prebronchodilator forced expiratory volume in 1 second, type 2 inflammatory biomarkers over 52 weeks, and the proportion of patients achieving asthma control (5-item Asthma Control Questionnaire score < 1.5), grouped by treatment (dupilumab or placebo plus medium- or high-dose ICS). RESULTS:Dupilumab improved clinical outcomes and reduced biomarker levels across ICS-dose subgroups. Dupilumab plus medium-dose ICS (n = 513) reduced exacerbations by 70% vs placebo plus high-dose ICS (n = 287) (P < .0001). At week 52, dupilumab plus medium-dose ICS improved prebronchodilator forced expiratory volume in 1 second by 0.22 L (P < .0001) and increased the odds ratio for achieving asthma control to 2.26 (P < .0001) vs placebo plus high-dose ICS. CONCLUSION:Add-on dupilumab with medium-dose ICS improved outcomes in patients with uncontrolled asthma compared with high-dose ICS and placebo. The QUEST study was not designed to compare add-on dupilumab with ICS dose escalation, but these findings from this post hoc analysis warrant future studies directly comparing ICS dose escalation with add-on dupilumab. TRIAL REGISTRATION:ClinicalTrials.gov Identifier: NCT02414854.

BACKGROUND:Wheezing lower respiratory tract illnesses are a major health concern in preschool children. We report the results of the ORBEX trial which evaluated the safety and efficacy of the bacterial lysate, OM-85, in the primary prevention of wheezing lower respiratory tract illness. METHODS:ORBEX is a parallel-arm, double-blind, placebo-controlled trial for the primary prevention of wheezing lower respiratory tract illness in young children at increased risk for asthma due to atopic dermatitis, parental asthma, or asthma in a blood sibling aged 4 years or older. Children aged 6-18 months were centrally randomly assigned (1:1) at 11 academic clinical sites with experience in recruiting young children in the USA to receive OM-85 3·5 mg or placebo orally for 10 days each month for 24 months and then followed for an additional 36 months to evaluate outcomes while they were off the study drug. Identical openable capsules were used for active drug and placebo, and staff, investigators, and participants were masked to treatment assignment. Participants received usual treatment for wheezing illness as per US guidelines. Randomisation was stratified by sex, age group, family history of asthma, and clinical site. The primary outcome was the time to first wheezing lower respiratory tract illness during the 36-month observation period off the study drug analysed in the intention-to-treat population, which included all randomly assigned participants. The trial is registered with clinicaltrials.gov, NCT02148796, and is completed. FINDINGS:Between Jan 3, 2017, and Nov 30, 2020, 984 children were screened for eligibility, 162 were excluded, and 822 were randomly assigned (411 to the OM-85 intervention group and 411 to the placebo group). 492 participants were male (59·9%) and 330 (40·1%) were female and the mean age of participants was 11·8 months (SD 3·8). 681 children completed the 24-month treatment period, and 596 children completed the 36-month observation period. 132 children experienced at least one wheezing lower respiratory tract illness during the observation period; 71 (21%) of 342 in the OM-85 group and 61 (18%) of 339 in the placebo group. There was no significant difference between OM-85 and placebo with respect to the time to first wheezing lower respiratory tract illness (log-rank test p value 0·35; hazard ratio 1·16 [95% CI 0·82-1·64]). The most frequent adverse events, fevers, coughs, and colds, did not differ between groups. INTERPRETATION:Oral administration of OM-85 in early life did not decrease the incidence of wheezing lower respiratory tract illness in this high-risk population. Bacterial lysates are not efficacious for the primary prevention of asthma-like symptoms during the preschool years. FUNDING:National Heart, Lung, and Blood Institute and OM Pharma with supplemental funding and provision of study drug and placebo from OM Pharma.

Background and Purpose: Children with acute asthma exacerbations are frequently hospitalized due to insufficient response to inhaled β-agonist and systemic corticosteroid potentially due to leukotriene mediated airway inflammation. Montelukast is a potent leukotriene receptor antagonist approved for chronic asthma treatment. We performed a randomized dose-escalation trial of high-dose oral montelukast to identify the dose of oral montelukast suitable for future efficacy studies. Experimental Approach: We performed a Phase 2, adaptive, double-masked randomized controlled trial comparing high-dose oral montelukast plus standard treatment versus standard alone in children with exacerbations moderate-to-severe exacerbations after initial inhaled albuterol treatment. Three sequential groups received escalating weight-based dose levels (2.0, 2.5, and 3.0 mg/kg) with maximum plasma concentration (Cmax) used as the pharmacokinetic target for dose escalation. We hypothesized that at least one dose level would achieve a target Cmax of 1,700 ng/ml in > 86% of dose-level participants. Key Results: Among 45 participants randomized to montelukast and 44 to placebo, median [IQR] ages were 6.6 [5.4, 10] and 6.7 [5.3, 9.9] years, with high-moderate pre-treatment exacerbation severity. The target Cmax was reached in 67%, 80%, and 90% of participants at doses of 2.0, 2.5, and 3.0 mg/kg, respectively. Adverse events were infrequent and mild. Conclusion and Implications: Among children with moderate or severe acute asthma exacerbations not responsive to initial inhaled albuterol, oral montelukast at a dose of 3.0 mg/kg reliably achieves a potentially therapeutic Cmax. These findings support dose selection for an adequately powered efficacy trial of montelukast in this population.

BACKGROUND:The benefits and harms of using macrolides for asthma remain unclear. OBJECTIVE:As part of upcoming Academy of Allergy, Asthma and Immunology/American College of Allergy, Asthma and Immunology Joint Task Force on Practice Parameters guidelines addressing severe asthma, we systematically reviewed the efficacy and safety of macrolides for asthma. METHODS:We systematically searched MEDLINE, Embase, and CENTRAL to April 12, 2025, for randomized trials comparing macrolides with placebo or standard care for asthma. Paired reviewers independently screened records and extracted data. Individual patient-level data in random effects analysis of covariance models addressed asthma control and asthma-related quality of life. Random effects meta-analyses addressed severe exacerbations and harms. We used the Grading of Recommendations Assessment, Development and Evaluation approach to evaluate certainty of evidence. Our study protocol is registered in PROSPERO (CRD42023408677). RESULTS:Our meta-analysis comprised 19 trials enrolling 1825 participants. Compared with placebo, macrolides improve asthma control (6-item Asthma Control Questionnaire; score range 0-6, lower better; between-group mean difference: -0.23 [95% CI -0.32 to -0.13]; 40.6% vs 21.6% improving by minimally important difference of 0.5 point; high certainty), likely reduce severe exacerbations (incidence rate ratio: 0.75 [95% CI 0.57 to 0.98]; rate difference: 0.26 fewer events per patient-year [95% CI 0.45 to 0.02 fewer events]; moderate certainty), and likely modestly improve quality of life (Asthma Quality of Life Questionnaire; score range 1-7, higher better; mean difference: 0.11 [95% CI -0.06 to 0.29]; 47.6% vs 42.4% improving by minimally important difference of 0.5 points; moderate certainty) with little to no effect on serious adverse events and mortality (high certainty). Relative effects were similar among patients with type 2 high inflammation versus type 2 low inflammation asthma. CONCLUSIONS:Macrolides likely reduce severe exacerbations and improve asthma control and quality of life with little to no difference in serious harms among patients with type 2 high inflammation or type 2 low inflammation asthma.

Background The Global Initiative for Asthma recommends patients with asthma uncontrolled on medium-dose inhaled corticosteroid (ICS) plus long-acting β2-agonist (LABA) therapy to first escalate their ICS dose before considering add-on biologic therapy despite acknowledging that high-dose ICS provides little additional benefit for most patients and carries an increased risk of side effects. Dupilumab, an interleukin (IL)-4Rα antagonist that inhibits signaling of IL-4 and IL-13, has demonstrated efficacy in patients with uncontrolled moderate-to-severe asthma and type 2 inflammation. Objective The AIM4: Next Step study will evaluate whether earlier intervention with dupilumab provides clinical benefit compared with escalation to high-dose ICS/LABA. Methods AIM4: Next Step (NCT06572228) is a randomized, double-blind, active-controlled study enrolling approximately 250 adolescents and adults with type 2 inflammatory asthma uncontrolled with medium-dose ICS/LABA treatment. Patients will be randomized 1:1 to receive dupilumab 300 mg every 2 weeks plus medium-dose ICS/LABA or placebo plus high-dose ICS/LABA. Results The primary endpoint is the annualized rate of severe asthma exacerbations over 52 weeks. Key secondary endpoints include change from baseline in pre-bronchodilator forced expiratory volume in 1 second at week 12, annualized systemic corticosteroid exposure for exacerbations, and asthma control at week 12 based on 5-item Asthma Control Questionnaire. Conclusion AIM4: Next Step is the first study designed to address an important gap in asthma management by directly comparing ICS dose escalation versus early biologic intervention with dupilumab in patients with uncontrolled type 2 inflammatory asthma. Findings may inform future treatment strategies for patients whose asthma remains uncontrolled despite ICS/LABA.

Background:The efficacy and safety of bronchial thermoplasty (BT) for severe asthma remains unclear. Objective:We systematically synthesized the efficacy and safety of BT in patients with severe asthma. Methods:As part of the upcoming American Academy of Allergy, Asthma & Immunology/American College of Allergy, Asthma & Immunology Joint Task Force on Practice Parameters severe asthma guidelines, we searched the Medline, Embase, and Central databases to July 29, 2025, for randomized trials comparing BT to control for asthma. Paired reviewers independently screened records and extracted data. Random-effects meta-analyses addressed asthma control (Asthma Control Questionnaire 6 [scale, 0-6; lower better]), asthma-related quality of life (Asthma Quality of Life Questionnaire [range, 1-7; higher better]), severe asthma exacerbations, and harms, stratified by procedural, postprocedural, and overall. The GRADE approach informed certainty-of-evidence ratings (PROSPERO: CRD42023408565). Results:Six trials randomized 573 adults. Procedurally, BT likely increases severe exacerbations (incidence rate ratio [IRR] 2.95; 95% CI, 1.20-7.25; risk difference [RD] 0.08 more events per patient-year; moderate certainty) and serious respiratory adverse events (IRR 5.98; 95% CI, 1.07-33.29; RD 0.18 more events per patient-year; moderate certainty). Postprocedurally, BT may reduce severe exacerbations (IRR 0.67; 95% CI, 0.50-0.89; RD 0.67 fewer events per patient-year; low certainty). Overall, BT may improve asthma control (mean difference -0.37; 95% CI, -0.67 to -0.07; RD for 0.5-point decrease: 15.9% more; low certainty), asthma-related quality of life (mean difference 0.55; 95% CI, 0.28-0.82; RD for 0.5-point increase: 19.1% more; low certainty), and severe exacerbations (IRR 0.81; 95% CI, 0.68-0.97; RD 0.11 fewer events per patient-year; low certainty). Conclusion:Among adults with severe asthma, BT may improve asthma control and asthma-related quality of life and may reduce overall severe exacerbations, but it likely increases procedural severe exacerbations and serious respiratory harms.

Background Single-nucleotide polymorphisms (SNPs) in the chromosome 17q12-q21 region and, independently, early-life nasal microbiota dominated by Moraxella, Streptococcus, or Haemophilus (MSH) increase risk of chronic wheeze and asthma development. Objective We sought to determine whether 17q12-q21 risk SNPs and nasal microbiota interact to modulate childhood wheeze risk. Methods Nasal wash samples from 12-month-old infants in 2 birth cohorts, COAST (Childhood Origins of Asthma; n = 180) and URECA (Urban Environment and Childhood Asthma; n = 139), underwent 16S ribosomal RNA variable region 4 sequencing. Nasal microbiota dominated by MSH or Corynebacterium, Dolosigranulum, Staphylococcus, or Bacillus (CDSB) were assessed. Paired blood was genotyped for 9 17q12-q21 risk SNPs. Logistic regression tested interactions between 17q12-q21 SNPs and MSH or CDSB on wheeze risk in the first 3 years of life. A549 lung epithelial cells, CRISPR-edited to encode the rs7216389 risk genotype (rs7216389TT) were compared to the heterozygous (rs7216389CT) line using bulk RNA sequencing. Results SNPs, particularly those in the ORMDL3 (rs8076131; odds ratio [OR]: 1.72; 95% CI: 1.09-2.71; Pint = .031) and GSDMB (rs2305480; OR: 1.72; 95% CI: 1.09-2.71; Pint = 0.042; and rs7216389; OR: 1.73; 95% CI: 1.09-2.70; Pint = .047) genes, interact with MSH microbiota to increase early-life wheeze risk (false discovery rate Pint = .016 for all), while interactions with CDSB reduce risk. A549 airway epithelial cells homozygous for rs7216389TT exhibited decreased expression of genes involved in antimicrobial responses and neutrophil recruitment and evidence increased microbial adherence compared with the heterozygous cell line. Conclusion Airway microbiota interact with SNPs at the 17q12-q21 locus in genes involved in sphingolipid metabolism and intracellular antimicrobial responses, to modulate wheeze risk.

BACKGROUND:DNA methylation accurately predicts chronological age, including gestational age (GA). Previous studies have used 5'-C-phosphate-G-3' sites (CpGs) on the EPIC or 450K arrays to generate epigenetic clocks for estimating GA. OBJECTIVE:Using the Asthma&Allergy array, we estimated GA and calculated GA acceleration (GAA) in cord blood DNA from 2451 ancestrally diverse participants from 7 birth cohorts investigating early life risk factors for asthma and allergic diseases and disease onset in childhood. METHODS:Two gestational epigenetic clocks were constructed: one used GA-associated CpGs in an epigenome-wide association study (EWAS) and a second used CpGs associated with GA in specific cell types. For both, we calculated GAA and tested for associations with 6 prenatal variables and 8 allergy-related childhood outcomes. We then conducted pathway analysis of expressed genes correlated with GAA and validated gene expression signatures in peripheral blood at age 2 years. RESULTS:Strong correlations between reported GA and estimated GA were observed using the EWAS and the cell-specific clocks (r = 0.90 and 0.83, respectively). Using the cell-specific clock, GAA was associated with 2 outcomes (higher birthweight, Padj = 1.69 × 10-5; less allergic asthma, Padj = .025), while the EWAS clock was associated with birthweight (Padj = 4.68 × 10-4). A significant sex-by-GAA interaction effect on birthweight, with a larger effect size in females, was observed with both clocks (EWAS, Pint = 5.77 × 10-3; cell-specific, Pint = .021). Cord blood RNA-sequencing analysis revealed upregulated IL6 and TNF and downregulated IL10 signaling pathways associated with GAA, and gene expression in blood at age 2 years further revealed associations with asthma at age 7 years. CONCLUSION:Positive correlations between GAA and inflammatory gene expression and the negative association with allergic asthma suggest that increased expression of inflammatory genes in cord blood and at age 2 years is protective against developing asthma. CpGs on the Asthma&Allergy array are accurate predictors of GA, capturing aging aspects specifically related to inflammatory programs.