Our previous studies demonstrated that C66 inhibits inflammation, fibrosis, and oxidative stress, which is accompanied by JNK activity inhibition.10, 11 Evidence has shown that JNK2 activation increases metabolism‐related inflammation, fibrosis, and oxidative stress.12, 13, 14 Consistent with these findings, our present study demonstrated that both C66 treatment and JNK2 knockout markedly reduced diabetic‐induced cardiac inflammation, fibrosis, and oxidative stress; however, C66 had no effect on JNK2−/− diabetic mice. Here, MAPK9 is linked to inflammatory response.