Our previous results indicated that Akt1 promotes enrichment of cancer stem cell-like cells and chemoresistance in HCC cells [11], but despite numerous studies pointing to Akt as a primary transducer of the PI3K signal, PIK3CA mutant tumors have strikingly low levels of phosphorylated (activated) Akt, indicating that other effectors must link PI3K to tumorigenesis [12]. This evidence concerns the gene AKT1 and hepatocellular carcinoma.