Nonenzymatic modification of protein by cyanate, that is, carbamylation, has received new attention due to its apparent relevance in atherosclerosis. For example, carbamylation of low-density lipoprotein (LDL) is an important mechanism that potentially impacts high-risk atherosclerotic individuals with increased urea (renal insufficiency) or thiocyanate (tobacco smoking). Carbamylated LDL (cLDL) is increased in patients with end-stage kidney disease, especially those with atherosclerosis. In addition, cLDL exhibits distinct cytotoxic effects when tested in vitro on endothelial cells, induces the expression of adhesion molecules, and aggravates the monocyte adhesion to endothelial cells. It also facilitates the proliferation of vascular smooth-muscle cell (VSMC). Studies of potential pharmacological interruption of these processes in vivo may lead to discoveries of novel therapies for atherosclerosis.