The complement pathway has not been previously linked to increased cardiovascular risk in OSA; however, CD59 deficiency promotes MAC deposition and accelerates atherosclerosis in ApoE−/− and Ldlr−/− mice (29, 30), whereas selective overexpression of human CD59 in the endothelium and hematopoietic cells renders ApoE−/− mice resistant to atherogenesis (31). The gene discussed is LDLR; the disease is atherosclerosis.