The idea that RIPK3 signals through CaMKII instead of MLKL in cardiomyocytes and perhaps other cell types is interesting and has also been investigated by Chang et al. who demonstrated elevated CaMKII phosphorylation in acute myocardial infarction and tunicamycin-induced cardiomyocyte necroptosis, alongside unaltered levels of MLKL [12]. This evidence concerns the gene RIPK3 and acute myocardial infarction.