Mice deficient in RIPK3 (Ripk3−/−) had significantly smaller infarct sizes compared to wild-type mice 3 days after MI, and significantly improved ejection fractions (45 ± 3.6 vs. 32 ± 4.4%, p < 0.05) and a lesser degree of cardiac hypertrophy compared to control peers 30 days after experimental left anterior descending coronary artery ligation [31,35]. Here, RIPK3 is linked to myocardial infarction.