Opposite to p53, PI3K/Akt/NF-κB pathway is one of the most frequently over-activated intracellular pathways and involved in anti-apoptosis in various cancers, while PTEN inhibits PI3K/Akt signaling pathway.19,20 In apoptosis, Bcl-2 can interact with Bax on the mitochondrial membrane to suppress Bax-mediated opening of the mitochondrial voltage-dependent anion channel for apoptosis.21 In esophageal cancer cells, KRT80 silencing ameliorated proliferation and induced the apoptosis by inactivating PI3K/Akt/NF-κB, up-regulating PTEN and p53 or decreasing Bcl-2/Bax. This evidence concerns the gene AKT1 and esophageal cancer.