In this study, the hydrodynamic transfection of a mutated form of PI3K subunit alpha alone into mouse livers led to hepatic steatosis, whereas the transfection with a combination of a mutated form of PI3K subunit alpha combined with either NRASV12 or c-Met in the mouse liver led to the development of tumor nodules, which exhibited an increase in the activation of Akt/mTOR and RAS/MAPK signaling pathways. The gene discussed is PIK3CA; the disease is fatty liver disease.