Indeed, the reductions in atherosclerotic plaques in LDLR−/− mice upon treatment with glutaminase or ACLY inhibitors as well as in LDLR−/− mice harboring LysM-Cre ACLYf/f bone marrow support the importance of glutamine catabolism and oxaloacetate accumulation in atherosclerosis [226, 262]. The gene discussed is LDLR; the disease is atherosclerosis.