As we expected, the enhanced activity of AKT by bpV(HOpic) could significantly reduce heart tissue damage (Figure S10), and cardiac apoptosis combined with increase of FOXO3A and pro‐apoptotic genes BIM/PUMA as well as decrease of BCL‐2 in the Kcnh2+/‐ heart when challenged with LPS(Figure 6E‐F), that may be why AKT, at least, is one of potential regulators in FAK pathway to mediate the effect of Kcnh2 in protecting heart from sepsis damage. This evidence concerns the gene FOXO3 and Sepsis.