Absence of CD40-TRAF6 interactions in MHCII+ cells hampered leukocyte recruitment to the plaque, reduced immune cell abundance within the plaque and limited polarization and activation of M1 macrophages, indicating that CD40-TRAF6 interactions predominantly promoted monocyte/macrophage-driven inflammation in atherosclerosis [25]. The gene discussed is CD40; the disease is atherosclerosis.