The unique molecular mechanisms detailed previously—the “imprinting” of the PI3K/Akt/mTOR pathway and the “synergistic amplification” of immune evasion—are not just of academic interest; they profoundly impact the response to current HCC therapies and provide a clear rationale for the clinical challenges observed in the MASH-HCC subtype. The gene discussed is MTOR; the disease is hepatocellular carcinoma.