Mechanistically, the deletion of STING not only attenuates expression of p-TBK1 and p-IRF3, but also alleviates the expression of p-PERK, p-IRE1α and p-eIF2α, so, in cardiac hypertrophy, STING could mediate ER stress through phosphorylating PERK and eIF2α (143). This evidence concerns the gene STING1 and cardiac hypertrophy.