Contemporarily, in an era of improved control of traditional risk factors, endothelial erosion appears to account for as high as one‐third of acute coronary syndromes.[30] As reported, IFN‐I and the downstream JAK‐STAT1 signaling directly induce EC dysfunction.[31, 32] Moreover, CKD is closely associated with EC dysfunction.[33] In the uremic milieu, IFN‐I response may also induce endothelial erosion and contribute to the increased risk of cardiovascular events in patients with CKD. The gene discussed is STAT1; the disease is acute coronary syndrome.