AKT1 and hepatocellular carcinoma: Liu et al. [62], through in vivo preclinical studies performed on transgenic mice characterized by overexpression of SRY and treated with N-diethylnitrosamine (DEN, a promoter of HCC development), indeed showed that overexpression of SRY in male mice promoted hepatocarcinogenesis in 84% of male mice, activating the Sox9 and PDGFRα/PI3K/Akt pathway.