It should be noted that liver-specific Akt2 knockout inhibited hepatic TG accumulation either in ob/ob mouse or upon feeding high fat diet (HFD), and a hepatocyte-specific Pik3ca transgenic mouse developed steatosis and HCC, further establishing the importance of the activation of the PI3K/Akt pathway in NASH and NASH-HCC [147,148]. The gene discussed is AKT2; the disease is metabolic dysfunction-associated steatohepatitis.