These models allow for detailed investigation of cancer biology, including the interaction between tumor cells and their microenvironment through key signaling pathways such as PI3K/Akt, MAPK, and TGF-β, which exhibit bidirectional feedback with specific epigenetic modifiers, collectively regulating phenotype, proliferation, pluripotency, and chemoresistance. The gene discussed is AKT1; the disease is neoplasm.