Cyanate is a uremic toxin responsible for the carbamylation of proteins, which has been implicated as playing a key role in accelerating the progression of atherosclerosis in patients with chronic kidney disease. El-Gamal et al. report that while cyanate promotes protein carbamylation in vivo, the resulting endothelial dysfunction observed is consistent with reactions mediated by cyanate itself, rather than by carbamylated proteins. This provides new insight into the relationship between uremia and cardiovascular disease.