In concert with induction of factor XIIIA gene expression and protein in monocytes by cardiovascular risk factors (30), the consecutively exaggerated intracellular factor XIIIA activity accounts for covalent stabilization of AT1 receptor dimers, which are triggered by increased circulating angiotensin II levels in patients “at the onset of atherosclerosis” (30–32). The gene discussed is F13A1; the disease is atherosclerosis.