AKT1 and hepatocellular carcinoma: The experiments herein provide evidence that sublethal heat stress induced PI3K/mTORC2-dependant AKT signaling is a central mediator of HCC cell survival to thermal ablation induced heat stress in diverse molecular prognostic subtypes of HCC, thereby providing a mechanistic basis for adjuvant AKT inhibition as a therapeutic strategy to enhance thermal ablation induced HCC cell killing and prevent local recurrence, particularly at the ablation margin.