Finally, RIPK3 deficiency and RIPK3 inhibition were highly consistent, both resulted in reduced CaMKII activity, corrected the CaMKII δ alternative splicing disorder, alleviated oxidative stress, reduced necroptosis, and reversed myocardial injury caused by angiotensin-induced myocardial hypertrophy in mice. Here, CAMK2G is linked to cardiac hypertrophy.