Based on the observed increased number of IL‐33+ ECs within both the aortic adventitia and the internal thoracic artery of RA patients, one might speculate that this phenomenon could lead to a generalized endothelial dysfunction and impairment of microvascular function, which is likely to contribute to both RA‐specific manifestations (such as synovitis and extraarticular manifestations) and the pathogenesis of ischemia (due to both macrovascular and microvascular disease) and heart failure. The gene discussed is IL33; the disease is endothelial dysfunction.