The involvement of PTEN (phosphatase and tensin homolog) down-regulation in liver diseases predisposing to human HCC, such as NASH (non-alcoholic steatohepatitis), HCV hepatitis, and HCC [130], suggests a deregulation of PI3K/AKT/mTOR signaling. This evidence concerns the gene AKT1 and metabolic dysfunction-associated steatohepatitis.