TLCD3B and neoplasm: As bioactive mediators of cellular proliferation and apoptosis, ceramide metabolic perturbations (e.g., altered ceramide synthase activity) have been mechanistically linked to gastric oncogenesis.[32] Notably, ceramides exert tumor-suppressive effects through autophagic flux modulation and intrinsic apoptosis pathway activation, positioning sphingolipid metabolism as a promising therapeutic frontier.[33] These pleiotropic functions underscore ceramide’s potential as both a diagnostic biomarker and molecular target for GC interception strategies.