First, this study has provided both in vivo and in vitro evidence to identify a key signaling role for myokine CHI3L1 and its receptor PAR2 in promoting exercise training-elicited revascularization in the post-MI myocardium, which represents a new mechanistic explanation for a previously revealed phenomenon on cardiac angiogenesis-promoting effects of exercise in post-MI failing rat hearts [41]. This evidence concerns the gene CHI3L1 and myocardial infarction.