The investigators have postulated that in the absence of ACKR3/CXCR7, circulatory CXCL12/SDF1α, although it has its regenerative attributes, could affect post-MI cardiac remodeling [27] by engaging CXCR4, which is known to mediate fibrotic consequences. The gene discussed is CXCL12; the disease is myocardial infarction.