Similar anti-inflammatory effects associated with activation of HCAR2 in macrophages were demonstrated in a model of atherosclerosis in chimeric mice reconstituted with wild-type vs. HCAR2-deficient bone marrow, where the strong lipid-independent inhibitory effect of nicotinic acid on the progression of atherosclerosis was shown to be mediated by its receptor HCAR2 on bone marrow-derived cells [29]. The gene discussed is HCAR2; the disease is atherosclerosis.