Continuous monocyte recruitment into the vessel wall is one of the major steps in the pathogenesis of atherosclerosis, as evidenced by studies showing that simultaneous inhibition of CCL2, CX3CR1 and CCR5 near abolishes development of atheroma in ApoE−/− mice.36 In addition, deficiency of MIF also impairs atheroma development in low‐density lipoprotein‐receptor deficient mice37 an inhibitory anti‐MIF antibody has been shown to prevent atherosclerosis in ApoE−/− mice,38 and our previous work illustrated that MIF secretion was important. The gene discussed is APOE; the disease is atherosclerosis.