Current therapies of inflammatory bowel disease (IBD) predominantly target single inflammatory pathways and often fail to resolve oxidative stress or restore mucosal homeostasis, resulting in suboptimal clinical outcomes. Here, we report a biomimetic nano-biohybrid platform that integrates multifunctional nanozymes with probiotic-derived extracellular vesicles for synergistic treatment of IBD. In this system, a Cu/Zn bimetallic nanozyme with superoxide dismutase- and catalase-mimetic activities is engineered to achieve efficient reactive oxygen species (ROS) scavenging, while extracellular vesicles derived from Faecalibacterium prausnitzii provide intrinsic intestinal targeting, mucus penetration capability, and immunomodulatory bioactivity. Thus, in a colitis model, the hybrid system markedly alleviates disease severity, as evidenced by improved body weight recovery, reduced disease activity index (DAI), and restoration of colon length. In addition, this treatment significantly suppresses ROS accumulation, downregulates pro-inflammatory cytokines, and promotes epithelial barrier repair by upregulating tight junction proteins. These results indicated that our work establishes a multifunctional therapeutic strategy that integrates nanocatalytic ROS regulation with microbiota-derived biological signaling, providing a promising platform for precision intervention in IBD and other inflammation-associated diseases.

ObjectivesEsophageal leiomyosarcoma (ELMS) is an extremely rare malignant tumor, and the possibility of malignant transformation from benign esophageal leiomyoma has historically been dismissed. This report presents, to our knowledge, the first documented case of malignant transformation within an esophageal leiomyoma and its successful treatment via endoscopic submucosal dissection (ESD), challenging the conventional belief regarding the absolute benignity of esophageal leiomyomas.Case summaryA 52-year-old female presented with non-specific symptoms and was found to have a small (0.8 cm) esophageal submucosal nodule during gastroscopy. Endoscopic ultrasound (EUS) showed a well-defined hypoechoic lesion originating from the submucosal layer. The lesion was completely resected via ESD. Histopathological examination demonstrated a conventional leiomyoma with a focal area of malignant transformation to leiomyosarcoma, characterized by high cellularity, nuclear atypia, increased mitotic activity [5 per 2 high-power fields (HPF)], elevated Ki-67 index (40%), and loss of smooth muscle markers (SMA, desmin) in the malignant region. Surgical margins were tumor-free. The patient recovered well with no recurrence at 60-day follow-up.

This corrects the article on p. 279 in vol. 26, PMID: 41942360.

Background: Endoscopic submucosal dissection (ESD) of superficial esophageal squamous cell carcinoma (SESCC), with or without the esophageal gland duct involvement (DI or NDI), has been reported in small case series, but ESD-related safety, efficacy, and outcomes remain unknown. We conducted a retrospective study of those issues in consecutive 748 patients treated at our center in China. Material and Methods: Over the study period from January 2014 to January 2019, we identified 748 eligible SESCC patients who were divided into the DI (22.6%, 169/748) and NDI (77.4%, 579/748) groups, based on histopathologic reports. Following the European and Japanese guidelines on endoscopic resection of SESCC, we investigated and statistically compared characteristics of clinicopathology and ESD-related safety, efficacy, and prognosis between DI and NDI groups. Results: The mean age of patients was 64.9 years for the cohort and significantly older in the DI (66.1) than in the NDI (64.5) group (P<0.05). There was no significant difference in smoking/alcohol abuse and comorbidity. Endoscopically, the DI group showed significantly larger tumor size and deeper invasion than the NDI group. There was no ESD-related death in the cohort. Although the en bloc resection rate was 100%, the complete and curative resection rates were significantly lower in the DI (88.2% and 61.2%, respectively) than in the NDI (96.4%, and 86.9%, respectively) group (P<0.01). ESD-related infection (0.7%) and bleeding (2.3%) rates were very low and no significant difference was found between the two groups. Only one perforation (0.1%) occurred in the NDI group. Post-ESD stenosis was 11.9% for the cohort and significantly more common in the DI (20.7%) than in the NDI (9.3%) group (P<0.01). The overall survival rate was 95.7% for the cohort and significantly lower in the NDI (94.6%) than in the DI (100.0%) group (P<0.05). However, there was no significant difference in disease-specific death, recurrence-free survival, distant metastasis, and the requirement for subsequent chemoradiation therapy and surgery between the two groups. Conclusion: In our cohort, there was no ESD-associated death; ESD-related infection and bleeding were minimal; and perforation was rare. Post-ESD stenosis was 11.9% in prevalence and successfully managed by endoscopic dilation. The overall survival rate was 95.7%. Compared to the NDI group, the DI group showed older age, larger tumor size, deeper invasion, lower complete and curative resection rates, higher prevalence of post-ESD stenosis; there was no significant difference in disease-specific death. Taken together, ESD was safe with excellent efficacy and prognosis for endoscopic resection of SESCC with or without esophageal gland duct involvement. Keywords: superficial esophageal squamous cell carcinoma, endoscopic submucosal dissection, ductal involvement, survival, postoperative stenosis.

‘Liver injury-liver fibrosis/cirrhosis-liver cancer’ is the key evolution pathway of hepatocellular carcinoma (HCC), chronic inflammation serving as a major driving force in this process. However, the regulatory mechanisms underlying this process require further clarification. Here, the carcinogen-induced liver injury, liver fibrosis, and HCC models were investigated in the wild-type and STK39-knockout mice. Mass spectrometry analysis and immunoprecipitation assays were used to identify the interaction factors of STK39. QPCR, ELISA, and immunofluorescence were applied for the expression of inflammatory factors. In this study, we report that STK39 is gradually upregulated during the evolution of HCC (liver injury-liver fibrosis-liver cancer). Consequently, overexpression of STK39 further encouraged the evolution of HCC by facilitating a macrophage inflammatory response, as demonstrated in carcinogen-induced liver injury, liver fibrosis, and HCC models. Pharmacological inhibition of STK39 significantly slows the progression of HCC; however, this effect was considerably diminished after macrophage clearance. Mechanistically, mass spectrometry analysis and immunoprecipitation assays identified that STK39 interacted with PKR and promoted the activation of the PKR/NF-κB axis. Which, in turn, enhanced the macrophage inflammatory response and accelerated the evolution of HCC. The inflammatory factor TNF-α further induces the expression of STK39, suggesting a positive feedback regulation process exists. More notably, STK39 inhibition improves the efficacy of sorafenib and anti-PD1 therapy. In conclusions, our study reveals that STK39 holds significant potential for the early diagnosis and treatment of HCC.

BACKGROUND:Accurate prediction of lymph node metastasis (LNM) is crucial for treatment decisions in early gastric cancer (EGC). Current preoperative methods for LNM prediction are often insufficient. PATIENTS AND METHODS:This multicenter retrospective study enrolled 605 EGC patients who underwent endoscopic submucosal dissection (ESD) and/or surgery across five institutions between 2013 and 2023. We developed a deep learning model, LNMate, to predict LNM before ESD and evaluated its impact on endoscopists' diagnostic performance. We also conducted immunohistochemical (IHC) analysis on tissue samples from 32 patients. Additionally, we constructed a deep learning-based endoscopic nomogram (DLEN) to estimate LNM risk after ESD, validated through comparison with the eCura system. RESULTS:LNMate showed high predictive performance with area under the curves (AUCs) ranging from 0.843 (95% confidence interval [CI], 0.782-0.904) to 0.875 (95% CI, 0.814-0.936). With LNMate assistance, endoscopists improved diagnostic accuracy by 13.8%, particularly in specificity (mean increase of 0.17, P = 0.03). IHC analysis showed associations between CD8+ and CD20+ cell enrichment with non-LNM predictions, and CD68+ macrophage infiltration with LNM. The DLEN outperformed the eCura system (AUC, 0.91 [95% CI, 0.86-0.97] vs. 0.71 [95% CI, 0.58-0.83], P < 0.01), reducing oversurgery by 24.2%, with no false negatives. CONCLUSIONS:The deep learning-based intelligent system for the entire treatment process of EGC showed excellent performance in predicting LNM, offering valuable decision support for both endoscopists in pre-ESD treatment planning and surgeons in post-ESD surgical decision-making.

Background and aims: Atrophy extends beyond the cardia is open atrophy and closely related to gastric cancer. However, there is difficulty in determining cardia atrophy under endoscopy. Methods: This is multicenter prospective study, a total of 895 patients were assigned to the training and validation sets to establish a cardia atrophy diagnostic model. A total of 220 patients were included in the internal test set. Additionally, a total of 354 patients were included in the external test set. In the internal and external test sets, three senior and three junior endoscopists made online diagnoses, comparing the performance differences to the artificial intelligence (AI)-assisted system. Results: In the internal test dataset, the accuracy, sensitivity, and specificity of the AI-assisted cardia atrophy diagnostic system were 0.927, 0.941, and 0.919, respectively, with a positivev predictive value (PPV) of 0.878, negative predictive value (NPV) of 0.962, and area under the curve (AUC) of 0.967. In the external test dataset, the accuracy, sensitivity, and specificity were 0.918, 0.894, and 0.931 respectively, with a PPV of 0.874, NPV of 0.943, and AUC of 0.953. Furthermore, it was found that the diagnosis accuracy, sensitivity, specificity, PPV, and NPV of the AI-assisted system were all higher than those of senior endoscopists. The receiver operating characteristic curve area (AUC) of AI-assisted system was 0.967 and 0.953 in the internal and external test sets, respectively. Heat map showed a high consistency between the AI-system and endoscopists. Conclusion: Our newly developed AI-assisted system shows superior performance in identifying cardia atrophy compared to senior endoscopists, and can be used to guide endoscopic judgment and targeted biopsies for cardia atrophy.

Purpose: Due to the preservation of the entire stomach after endoscopic resection, the occurrence of metachronous gastric cancer (MGC) remains a possibility. In this study, we investigated the incidence and risk factors for MGC in patients with early gastric cancer who underwent endoscopic submucosal dissection (ESD) and successfully eradicated Helicobacter pylori. Materials and Methods: A retrospective analysis was conducted of 1,191 patients who underwent ESD and successfully eradicated H. pylori at the Affiliated Drum Tower Hospital of Nanjing University. Endoscopic surveillance was performed at 3, 6, and 12 months post-resection, and annually thereafter. MGC was defined as the development of a new cancer at a site other than the primary gastric cancer site, at least 1 year after the initial endoscopic resection. Results: A total of 77 patients were diagnosed with MGC during a median follow-up of 41.5 months. Kaplan-Meier analysis showed a 5-year cumulative incidence of MGC of 9.4% after successful H. pylori eradication. Multivariate analysis of the training set using Cox proportional hazards models identified male sex, severe atrophic gastritis, multiple gastric cancers before H. pylori eradication, and smoking history as independent risk factors for MGC. The nomogram exhibited favorable discrimination, with area under the curves of 0.767 and 0.822 in the training set and 0.724 and 0.745 in the testing set at 3 and 5 years, respectively. Conclusions: Patients with gastric cancer who undergo endoscopic resection, even after successful H. pylori eradication, should undergo annual and continuous endoscopic surveillance for MGC.

Tissue-resident memory T cells (TRM cells) have been shown to play an instrumental role in driving the onset and relapse of inflammatory bowel diseases (IBD). However, the underlying mechanism of TRM cells differentiation and its regulation in intestines remain to be unveiled. Mothers against decapentaplegic homolog 3 (SMAD3) is translocated from nucleus to membrane and activated in response to transforming growth factor beta (TGF-β), which is a key cytokine in the process of TRM cells polarization. Cysteine palmitoylation (S-palmitoylation) is a post-translational modification catalyzed by the DHHC family, regulating protein membrane associations. Genes associated with the classic SMAD3 signaling pathway, along with most genes in the DHHC family, were upregulated in TRM cells. Our study demonstrated that SMAD3 underwent reversible S-palmitoylation on Cys31 by DHHC6, leading to SMAD3 endomembrane recruitment and its subsequent colocalization with TGF-β receptor I (TGF-βRI) under TRM polarization conditions. The membrane recruitment of SMAD3 activated SMAD3 and subsequently upregulated the expression of its target genes, inducing the differentiation of TRM cells. In contrast, perturbation in DHHC6-induced palmitoylation with MYD-4 inhibited TRM cells differentiation and alleviated colitis in IBD model mice. Our work provides an example how the immune responses are regulated through the S-palmitoylation-dependent SMAD3 signaling in TRM cells differentiation and reveals protein S-palmitoylation as a potential target in IBD treatment, which could be of greater application considering the wide involvement of protein S-palmitoylation in the signal transduction in mammalian cells. The differentiation of TRM cells is promoted through TGF-β/SMAD3 pathway. The palmitoylation of SMAD3 on Cys31 by DHHC6 drives the membrane localization, the phosphorylation and the activation of SMAD3 under TRM polarization conditions. Inhibiting the differentiation of TRM cells by blocking palmitoylation of SMAD3 ameliorates colitis.

BACKGROUND:A significant association between increased age and an increased risk of metachronous gastric cancer (MGC) following curative endoscopic submucosal dissection (ESD) has previously been reported. AIM:To determine risk factors for the metachronous occurrence of early gastric cancer (EGC) in elderly individuals. METHODS:This retrospective cohort study comprised 653 elderly patients (aged ≥ 65 years) who underwent curative ESD for EGC between January 2014 and June 2020 at Nanjing Drum Tower Hospital. Comprehensive analyses were conducted to compare lifestyle habits, comorbidities, and Helicobacter pylori (H. pylori) infections as potential indicators. RESULTS:During a median follow-up of 38 months, 46 patients (7.0%, 20.46/1000 person-years) developed MGC in the elderly cohort. The cumulative incidences of MGC at 2, 3, and 5 years were 3.3%, 5.3%, and 11.5%, respectively. In multivariate Cox regression analyses, the independent risk factors for MGC included metabolic dysfunction-associated steatotic liver disease (MASLD) [hazard ratio (HR) = 2.44, 95% confidence interval (CI): 1.15-5.17], persistent H. pylori infection (HR = 10.38, 95%CI: 3.36-32.07), severe mucosal atrophy (HR = 2.71, 95%CI: 1.45-5.08), and pathological differentiation of EGC (well/moderately differentiated vs poorly differentiated: HR = 10.18, 95%CI: 1.30-79.65). Based on these risk factors, a risk stratification system was developed to categorize individuals into low (0-1 point), intermediate (2-3 points), and high (4-8 points) risk categories for MGC, with cumulative incidence rates of 12.3%, 21.6%, and 45%, respectively. CONCLUSION:Among elderly individuals, MASLD, persistent H. pylori infection, severe mucosal atrophy, and well/moderately differentiated EGC were associated with an increased risk of MGC. Elderly patients are recommended to adopt healthy lifestyle practices, and undergo regular endoscopic screening and H. pylori testing after curative ESD for EGC.

RNA-binding proteins (RBPs) critically regulate post-transcriptional gene expression, yet their roles in chemotherapy resistance remain underexplored. Here, through a targeted siRNA screen of 40 RBM family members, we identified RNA-binding motif protein 8 A (RBM8A) as central orchestrator of oxaliplatin-induced DNA damage in gastric cancer (GC). Functional studies demonstrated that RBM8A promotes tumor proliferation and chemoresistance by recruiting the RNA helicase eIF4A3 to stabilize epidermal growth factor receptor (EGFR) mRNA, shielding it from exonucleolytic degradation. This stabilization sustains EGFR protein levels, enabling nuclear EGFR-DNA-PKcs complex formation to drive non-homologous end joining (NHEJ)-mediated DNA repair and suppress oxaliplatin-induced apoptosis. Therapeutic targeting of this axis with the EGFR inhibitor gefitinib restored oxaliplatin sensitivity in vitro and synergistically suppressed RBM8A-driven xenograft growth in vivo. Additionally, single-cell RNA-seq revealed RBM8A enrichment in malignant gastric epithelial cells, while tissue microarrays confirmed that dual RBM8A/EGFR overexpression predicts the poorest survival outcomes. Collectively, our findings define the RBM8A-eIF4A3-EGFR axis as a druggable determinant of chemoresistance and establish RBM8A as both a prognostic biomarker and therapeutic target in GC.

Diffuse gastric cancer (DGC) is characterized by high malignancy and metastasis rate, and poorly understood etiology, culminating in dismal patient outcomes. Here, through comprehensive analysis, we identified that glutathione peroxidase 2 (GPX2) plays a pivotal role in the progression of DGC by regulating lipid metabolism. This study demonstrates that GPX2 is markedly upregulated in DGC tissues, establishing its potential as an independent prognostic indicator. Functionally, GPX2 suppression disrupts lipid droplet formation and lipid homeostasis, leading to increased acylcarnitine levels that impair mitochondrial function. This disruption synergizes with endoplasmic reticulum stress to trigger apoptosis in gastric cancer cells. Notably, inhibiting GPX2 enhances the efficacy of cisplatin by sensitizing cancer cells to apoptosis. These insights identify GPX2 not only as a vital prognostic biomarker but also as a promising therapeutic target for overcoming cisplatin resistance in DGC, offering new avenues for treatment strategies.

Endoscopic electrosurgery faces critical challenges in achieving safe tissue dissection, particularly in procedures like endoscopic submucosal dissection (ESD). Current submucosal injection agents (e.g., normal saline) suffer from rapid diffusion requiring frequent reinjections that disrupt procedural continuity, while their poor electrical conductivity causes uneven current distribution and localized heat accumulation, increasing risks of tissue carbonization and iatrogenic perforation. Here a hydrogen bond-driven conductive thermosensitive hydrogel, poly(3,4-ethylenedioxythiophene):polystyrene sulfonate/Pluronic F127 (PEDOT:PSS/F127), is presented that overcomes these dual limitations through molecular engineering. The hydrogel integrates temperature-triggered gelation with enhanced mechanical strength (G' = 13.11 ± 0.22 kPa) via hydrogen bonding between F127's ether-oxygen and PEDOT:PSS's sulfonic groups. This synergy enables sustained mucosal elevation (> 60 min) while its embedded conductive phase optimizes electrosurgical current conduction. In vitro, ESD shows an 8.7 and 3 °C temperature reduction compared to saline and F127 controls, respectively. In vivo, PEDOT:PSS/F127 reduces tissue burns and bleeding, improving surgical safety. By addressing both mechanical instability and electrical limitations of conventional submucosal agents, this platform sets new standards for precision electrosurgery and demonstrates promising potential for a range of energy-based interventions.

Background: Metachronous gastric cancer (MGC) has gained increasing attention due to the preservation of the stomach during endoscopic resection for early gastric cancer (EGC). Objectives: This study aims to investigate the risk factors associated with MGC in the postoperative surveillance of endoscopic submucosal dissection (ESD). Design: A retrospective case-control study. Methods: The retrospective study was conducted between January 1, 2014, and June 30, 2020, at the Affiliated Drum Tower Hospital of Nanjing University Medical School. Results: Several independent risk factors for developing MGC were identified as smoking history (hazard ratio (HR) 2.39, 95% confidence interval (CI) 1.25–4.58), metabolic dysfunction-associated steatotic liver disease (MASLD; HR 2.44, 95% CI 1.23–4.87), cerebrovascular disease (CD; HR 2.55, 95% CI 1.09–5.99), multiple lesions (HR 2.06, 95% CI 1.17–3.63), Helicobacter pylori infection status (eradicated vs negative: HR 1.42, 95% CI 0.60–3.39; persistent vs negative: HR 5.47, 95% CI 2.13–14.03), and atrophic gastritis (AG; moderate vs mild: HR 4.44, 95% CI 1.36–14.53; severe vs mild: HR 7.30, 95% CI 2.11–25.22). The established nomogram based on these risk factors demonstrated high accuracy both in the training and test sets, with concordance indexes of 0.787, 0.762, and 0.845 for the training set, and 0.764, 0.824, and 0.788 for the test set at 2, 3, and 5 years, respectively. Conclusion: The risk factors for developing MGC after curative ESD for EGC were identified as smoking history, MASLD, CD, multiple lesions, H. pylori infection status, and AG. To reduce the risk of MGC, a healthy lifestyle, regular H. pylori testing, and annual endoscopic screening are recommended.

While much attention has been focused on the direct cytotoxic effects of anticancer agents on tumor cells, emerging evidence suggests that the induction of immunogenic cell death (ICD) and the consequent remodeling of the tumor microenvironment may critically influence overall therapeutic efficacy. Sorafenib, a multitargeted tyrosine kinase inhibitor, can induce ferroptosis and thereby trigger ICD, offering the potential to overcome chemoresistance and coordinate systemic antitumor immunity. However, its therapeutic efficacy in colorectal cancer (CRC) remains limited, attributing to its low efficiency in inducing ICD. Herein, this study investigates combined sodium butyrate (NaB) and sorafenib in liposomal co-delivery system (LipNaB@Sor) at an optimal 1:1 M ratio in CRC. LipNaB@Sor synergistically amplifies sorafenib-induced ferroptosis and consequent ICD, concurrently activating antitumor immunity through dendritic cell maturation and cytotoxic CD8+ T cell recruitment. Mechanistically, IRF2-mediated Oasl2 downregulation activates the cGAS-STING pathway, augmenting DNA damage signaling cascades. In vivo validation demonstrates significant tumor suppression and prolonged survival without observable toxicity, establishing LipNaB@Sor as a translatable strategy to overcome therapy resistance in immunologically unresponsive CRC.

BACKGROUND:Endoscopic submucosal dissection (ESD) is increasingly used for treating early gastric cancer (EGC). Noncurative ESD often necessitates additional surgical intervention because of the high risk of lymph node metastasis (LNM), but the optimal post-ESD management remains controversial. METHODS:This study collected data from patients with EGC who underwent noncurative ESD at Nanjing Drum Tower Hospital between January 2014 and December 2021. Patients were divided into surgical and observation groups and stratified by eCura scores into low (0-1), intermediate (2-4), and high-risk (5-7) categories. A 1:1 propensity score-matched analysis was performed between the 2 groups. Receiver operating characteristic analysis was used to assess the eCura score's ability to predict LNM. Survival outcomes, including overall survival (OS) and disease-specific survival (DSS), were compared between groups. RESULTS:Among the 260 patients, 91 were included in each group. No significant differences in OS or DSS were observed between the groups overall or among low-risk and intermediate-risk patients. However, high-risk patients in the surgical group had significantly better 5-year OS rates than those in the observation group, whereas the difference in DSS was not statistically significant. The eCura score exhibited strong predictive accuracy for LNM (area under the curve, 0.835; sensitivity, 70%; specificity, 92%). The subgroup analysis suggested that postchemoradiotherapy and total gastrectomy might be associated with better prognosis, although the differences were not statistically significant. CONCLUSION:The eCura scoring system seems to be a valuable tool for guiding post-ESD management. Treatment decisions should be based on the individual characteristics and clinical factors of each patient. For carefully selected patients who are not suitable candidates for surgery, ESD may be a viable alternative treatment option.

Colonoscopic withdrawal time is crucial for achieving a high adenoma detection rate (ADR) and reducing post-colonoscopy colorectal cancer risk. Enhanced qualified mucosal observation improves ADR, but manual quantification of qualified mucosal observation time (QMOT) in routine is challenging. We developed an artificial intelligence (AI) system, QAMaster, for automatic QMOT calculation during colonoscopy withdrawal. QAMaster comprises two models: Model I for image quality analysis (trained with 57,235 images from 64 patients) and Model II for anatomical landmark identification (trained with 7712 images from 3013 patients). Patients were stratified by QMOT, and ADR was compared. The areas under the curve (AUC) of Model I were 0.980–0.991, and Model II were 0.977–0.997. Among 482 patients, ADR was 36.54

Tissue-resident memory T cells (TRM cells) have been shown to play an instrumental role in driving the onset and relapse of inflammatory bowel diseases (IBD). However, the underlying mechanism of TRM cells differentiation and its regulation in intestines remain to be unveiled. Mothers against decapentaplegic homolog 3 (SMAD3) is translocated from nucleus to membrane and activated in response to transforming growth factor beta (TGF-β), which is a key cytokine in the process of TRM cells polarization. Cysteine palmitoylation (S-palmitoylation) is a post-translational modification catalyzed by the DHHC family, regulating protein membrane associations. Genes associated with the classic SMAD3 signaling pathway, along with most genes in the DHHC family, were upregulated in TRM cells. Our study demonstrated that SMAD3 underwent reversible S-palmitoylation on Cys31 by DHHC6, leading to SMAD3 endomembrane recruitment and its subsequent colocalization with TGF-β receptor I (TGF-βRI) under TRM polarization conditions. The membrane recruitment of SMAD3 activated SMAD3 and subsequently upregulated the expression of its target genes, inducing the differentiation of TRM cells. In contrast, perturbation in DHHC6-induced palmitoylation with MYD-4 inhibited TRM cells differentiation and alleviated colitisin IBD model mice. Our work provides an example how the immune responses are regulated through the S-palmitoylation-dependent SMAD3 signaling in TRM cells differentiation and reveals protein S-palmitoylation as a potential target in IBD treatment, which could be of greater application considering the wide involvement of protein S-palmitoylation in the signal transduction in mammalian cells.