Homocysteine, a sulphur-containing non-structural protein aminoacid is a non-lipid factor in the pathogenesis of artheriosclerosis. The metabolism of homocysteine and the processes responsible for the high serum level of this aminoacid are described. The pathogenesis of artheriosclerosis depends directly or indirectly on high serum levels of homocysteine, which generate disorders in proteins, DNA and lipid methylation, changes the expresion of some genes and secretion of EDRF. Indirect effects of homocysteine mostly involve the generation of free radicals causing endothelium injury, proliferation of vacular smooth muscle cells and structural changes in the extracellular matrix. All these changes result in the generation of artheriosclerosis plates, hyperproliferation of vacular myocytes and changes in vasodilator and artheriotrombosis activities, which cause the progression of artheriosclerosis.