Our results also showed that the dual mutations of tp53 and pten greatly increased Akt phosphorylation and obviously induced the features of nonalcoholic steatohepatitis (NASH), including infiltration of inflammatory cells, collagen deposition, and abnormal lipid accumulation [7, 87], in tumours derived from liver tissues in zebrafish (Fig. 4d-g). The gene discussed is AKT1; the disease is metabolic dysfunction-associated steatohepatitis.