MyD88 deficiency in myeloid cells has been shown to inhibit macrophage recruitment and activation of the M1 system. In vivo and ex vivo studies have linked MyD88-dependent growth factors produced by endothelial cells to initiating inflammation and development of atherosclerosis by priming the monocytes in arterial and adipose tissues to differentiate into M1-proinflammatory macrophages instead of M2 anti-inflammatory macrophages. This evidence concerns the gene MYD88 and atherosclerosis.