The observation that sublethal heat stress induces rapid PI3K/mTOR dependent AKT signaling and that inhibition of PI3K/mTOR-dependent AKT signaling enhances heat stress induced HCC cell killing raises the question whether blockade of the entire PI3K-AKT-mTOR pathway vs. AKT alone mediates the increased HCC cell killing to heat stress. Here, AKT1 is linked to hepatocellular carcinoma.