Collectively, our data suggest that in RA patients, the adventitial microenvironment, characterized by higher levels of IL‐18 and TNF and higher expression of nuclear IL‐33 within microvascular ECs, together with increased levels of soluble ST2, amplify the proatherogenic nature of the vessel, which theoretically enhances the pathology of atherosclerosis. The gene discussed is IL33; the disease is atherosclerosis.