MLKL and myocardial infarction: Moreover, although MLKL is the most well-established substrate of RIPK3 in executing necroptosis in many cell types, RIPK3 has been also reported to mediate cardiomyocyte necroptosis through MLKL-independent mechanisms in myocardial infarction, doxorubicin-induced cardiotoxicity and tunicamycin-induced endoplasmic reticulum stress [17, 28].