Myc, amplified in up to 30% of HCC patients26,43, was the oncogenic driver used in two of these HCC preclinical models, in combination with either loss of Trp53 (mutated in up to 50% of HCCs44) or activation of AKT/PI3K/mTOR signaling pathway (activated in 50% of HCC patients45) through Pten deletion. This evidence concerns the gene MTOR and hepatocellular carcinoma.