MET, a classical receptor tyrosine kinase (RTK), exerts its functions mainly through its pivotal downstream executor in the phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)–AKT cascade.24 To determine whether MET-controlled liver cancer immunogenicity is mediated by the AKT signaling pathway, we introduced the AKT constitutively activated mutant T308D/S473D (AKT-DD) and repeated the experiments described above (Fig. 4a). This evidence concerns the gene AKT1 and liver cancer.