For example, in mice Tnfrsf11b can inhibit atherogenesis and promote fibrous cap formation,26,27,28 fibromodulin can promote LDL accumulation in plaques29 and Sfrp4 reduces inflammation, oxidative stress, and plaque formation.30,31 In humans, both SFRP4 and FMOD are related to ruptured plaques,44 but FMOD was reduced in ruptured vs. stable plaques while SFRP4 was unchanged, and TNFRSF11B serum protein levels are associated with increased extent and progression of atherosclerosis and events (reviewed in45). The gene discussed is TNFRSF11B; the disease is atherosclerosis.