Here we show that in the absence of NOS3, the levels of EMMPRIN positive intraplaque macrophages were significant, and correlated with extensive plaque burden, when compared to NOS3 expressing atherosclerotic mice, suggesting that NOS3 may prevent MMP-mediated atherosclerosis through EMMPRIN inhibition, as we evidenced in cardiac myocytes, showing that NO inhibited EMMPRIN mRNA expression by repressing the promoter region [5]. The gene discussed is NOS3; the disease is atherosclerosis.