As expected, our current results suggested that PK2, PKR1, and PKR2 expression was remarkably dampened both in diabetic mouse hearts and H9c2 cardiomyocytes exposure to HG, which further confirmed that a decrease in PK2 may be the main contributor to myocardial apoptosis in DCM. Here, PROKR2 is linked to familial dilated cardiomyopathy.