Further, SR-B1 aids the conversion of macrophages from the inflammatory M1 to the anti-inflammatory M2 phenotype, and reduces NF-κB, p38 and Janus kinase (JNK) signalling [57]; mice lacking SR-B1 show enhanced expression of inflammatory cytokines, and a genetic variant of this receptor has been associated with increased risk of coronary heart disease [58]. This evidence concerns the gene SCARB1 and coronary artery disorder.