Phosphorylation of Akt at the hydrophobic motif and the activation loop activates the kinase and promotes cell survival.40 Finally, Akt activates mTORC1 by phosphorylation of tuberous sclerosis complex 2 (TSC2) to regulate cell survival.22 Previous studies showed that PHLPP1 could directly dephosphorylate the hydrophobic motif of Akt (Ser473) to promote tumour cell survival.40 However, the majority of the studies on PHLPP1 have been conducted in cancer cells, with little information regarding the function of PHLPP1 in the heart, especially in diabetic heart. This evidence concerns the gene PHLPP1 and neoplasm.