Using new apolipoprotein E (ApoE)−/−/caspase-1−/− double knockout mice, they observed that (i) early hyperlipidemia induced caspase-1 activation in ApoE−/− mouse aorta; (ii) caspase-1−/−/ApoE−/− mice attenuated early atherosclerosis; (iii) caspase-1−/−/ApoE−/− mice had decreased aortic expression of proinflammatory cytokines and attenuated aortic monocyte recruitment; and (iv) caspase-1−/−/ApoE−/− mice had decreased EC activation, including reduced adhesion molecule expression and cytokine secretion. The gene discussed is CASP1; the disease is hyperlipidemia.