The core molecules of sphingolipid metabolism—ceramide (Cer) and S1P—regulate cell fate through the “sphingolipid rheostat” model: Cer inhibits tumor growth by activating pro-apoptotic pathways (e.g., mitochondrial apoptosis), while S1P promotes tumor proliferation, angiogenesis, and chemotherapy resistance by activating the PI3K/AKT pathway and inhibiting apoptosis and autophagy (26–28). Here, AKT1 is linked to neoplasm.