IHH is a clinically important exposure because it markedly promotes atherosclerotic lesions in the pulmonary arteries and aorta not only in Ldlr−/− mice but also in ApoE knockout (ApoE−/−) mice, another widely used atherosclerosis model (3, 4), thereby mimicking the adverse cardiovascular changes that occur in OSA patients (5). The gene discussed is APOE; the disease is atherosclerosis.