demonstrated that lack of CD73, another ectonucleotidase that converts AMP to adenosine, on CD4+ T-cells resulted in increased inflammatory tonus and impaired cardiac function after ischemia/reperfusion (33), and antagonizing C-X-C chemokine receptor type 4 (CXCR4) reduced scar size and attenuated cardiac remodeling after MI, through mechanisms related to augmented Treg accumulation in the infarcted region (34). Here, CD4 is linked to myocardial infarction.