Consistently, Petri et al. found that atherosclerosis progression was slowed down in Ldlr−/−;FPR2−/− mice compared to Ldlr−/− mice and accelerated in Ldlr−/−;FPR2−/− mice after a Ldlr−/−;FPR2+/+ mouse bone marrow transplantation, highlighting the involvement of ALX/FPR2-mediated pro-inflammatory signaling in atheroma-associated macrophages. The gene discussed is LDLR; the disease is atherosclerosis.