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. The gene discussed is PTK2; the disease is inflammatory bowel disease.