Therefore, we can only establish that a reduced antioxidant capacity associated with low HDL levels and SR-B1 deficiency and activation of pro-inflammatory cascades9 contribute to microvascular dysfunction, functional and structural rarefaction and the rapid development of ischemic cardiomyopathy and heart failure in SR-B1−/−/ApoER61h/h mice. The gene discussed is SCARB1; the disease is heart failure.