The decision by the co-Editor-in-Chief of Regulatory Toxicology and Pharmacology, Prof. Martin van den Berg, to retract the 2000 review article by Williams, Kroes, and Munro has elicited widespread criticism within the scientific community. Issued in late 2025, the retraction decision cites procedural concerns including potential ghostwriting, undisclosed conflicts of interest, and omission of certain unpublished studies, invoking Committee on Publication Ethics guidelines despite lacking evidence of fraud or scientific flaws. This editorial argues that the retraction decision involves editorial overreach and misapplication of the guidelines. The alleged omissions stemmed from proprietary data access limitations that were disclosed in the original paper. Subsequent reviews by several independent expert panels and regulatory authorities with access to all glyphosate data, including the studies cited by the retracting editor, reached similar conclusions. Claims of ghostwriting were previously investigated and found lacking, including a declaration by EFSA as to the clarity of the conflict disclosures. The retraction’s timing, reliance on litigation documents, and apparent biases that were not disclosed in the retraction notice raise questions of ideological interference. Absent substantive rebuttals based on scientific merit rather than speculative claims of inappropriate authorship and data access, this retraction decision sets a dangerous precedent for retroactive censorship, potentially chilling beneficial industry-academic collaborations and eroding trust in the integrity of scientific publishing. With the strongest conviction, we assert that retracting a paper without scientific flaws isn’t protection—it is censorship. We therefore call for the immediate reversal of this flawed and unjustified retraction to preserve trust in peer-reviewed literature.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasing in prevalence worldwide. Pathogenesis of MASLD has been considerably heterogenous. Increased hepatic de novo lipogenesis, adipose tissue dysfunction, genetic predisposition, epigenetic mechanism, and other related factors have been associated with the development and progression of MASLD. Patients with MASLD are at high risk of not only adverse liver-related outcomes, including hepatocellular carcinoma, but also cardiometabolic disease including type 2 diabetes mellitus. Weight loss is the cornerstone of therapy among the various treatments for MASLD to decrease hepatic fat accumulation and delay the progression of inflammation and fibrosis. Resmetirom and semaglutide are approved for the treatment of metabolic dysfunction-associated steatohepatitis with moderate to advanced fibrosis, and many drugs are under investigation. Careful attention should be paid to the screening of MASLD, and concerted efforts should be made to manage it appropriately.
Granulocyte-macrophage colony-stimulating factor (GM-CSF) is an integral pathogenic factor in inflammatory lung pathologies including asthma, COPD, and lung cancer. As a pro-inflammatory cytokine, GM-CSF triggers the division and stimulation of granulocytes and macrophages, exacerbating the inflammatory response and promoting lung tissue damage. GM-CSF is an essential factor in promoting the production of the corresponding cytokines, levelling the effect of local activity by stimulating the infiltration of immune cells and maintaining chronic inflammation. Therefore, its neutralization in many ways leads to the cessation of the progression and exacerbation of inflammation in the lungs of patients with corresponding pathologies. Inhibitory therapy associated with GM-CSF reduces the number of immune cells and activates them at the inflammatory focus. The use of neutralizing antibodies to treat an acute inflammatory process is promising because they relatively quickly neutralize the effect of pathogenic GM-CSF. However, the immunocyte response can also be inhibited at the level of formation. Therapy with GM-CSF inhibitors can significantly reduce acute inflammation but can lead to adverse changes in the innate immunity of the patient. This review highlights GM-CSF's dual function of GM-CSF as a pathogenic contributor and possible treatment targets.
