Our previous study revealed that PTEN inhibition restores IPostC-induced cardioprotection in diabetes, mainly through upregulating the PI3K/Akt signaling pathway and partially by upregulating the JAK2/STAT3 signaling pathway, ultimately activating the GSK-3β-mediated mitochondrial pathway; this suggests that PTEN is a target for restoring the effects of IPostC [27]. The gene discussed is AKT1; the disease is diabetes mellitus.