Concurrently, compensatory hyperinsulinemia induced by insulin resistance drives abnormal tumor cell growth and resistance to apoptosis through the PI3K/AKT/mTORC1 axis, while overproduction of IGF-1 further initiates the Mitogen-Activated Protein Kinase (MAPK) pathway, thereby enhancing tumor cells’ adaptability to the hepatic microenvironment (5). This evidence concerns the gene INS and neoplasm.