Compared with WT-NASH mice, ptpro−/− mice exhibited a significant increase in the levels of p-PI3K, p-AKT, and p-s6k, suggesting that activated Akt (S473) rather than AKT (T308) signaling results in autophagy deficiency and aberrant lipogenesis, which in combination promote hepatocarcinogenesis. This evidence concerns the gene AKT1 and metabolic dysfunction-associated steatohepatitis.