The underlying mechanism involves the GSDMB knockout-induced inactivation of FAK through PDGF-A-dependent pathways, leading to an upsurge in the formation of actomyosin stress fibers.48 FAK stands as a critical tyrosine kinase governing the transition of focal adhesions and their engagement with the cytoskeleton, whereas PDGF-A regulates FAK phosphorylation.488–491 These results suggest a role for GSDMs in the pathogenesis of IBD, but the functional mechanisms may differ among various cell types, warranting further investigation. This evidence concerns the gene PDGFA and inflammatory bowel disease.