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. This evidence concerns the gene RIPK3 and cardiac hypertrophy.