Experimental studies in mice have indicated that, in the absence of CETP activity, ADCY9 inactivation protects against atherosclerosis, potentially through decreased macrophage accumulation and proliferation in the arterial wall, as well as by improving endothelial function.13ADCY9 mediates β2-adrenoceptor signaling, and it has been suggested that an interaction between HDL/ApoA1 and ADCY9 on this signaling may be relevant to the apparent pharmacogenetic interaction observed in dal-OUTCOMES.14 The gene discussed is APOA1; the disease is atherosclerosis.