Apoptosis is the genetically regulated form of cell death that permits the safe disposal of cells at the point in time when they have fulfilled their intended biological function. Bcl-2 is a protein that can render cells relatively resistant to induction of apoptosis by a wide variety of stimuli. Hyperglycemia negatively affects beta-cell mass by inducing apoptosis and it can also trigger apoptosis in tubular epithelial cells, retinal pericytes, cells of the dorsal root ganglion and the myocardium. High glucose mediated apoptosis is associated with down regulation of Bcl-2 gene expression. This study was designed to estimate the serum Bcl-2 level as a marker of apoptosis in type II diabetes. Blood samples from 80 subjects (Diabetics without vascular complications, n = 20; Diabetics with vascular complications, n = 40 and control subjects, n = 20) were taken and subjected to estimation of serum Bcl-2 level, percent of glycated Hb and other routine laboratory investigations. Results: Serum Bcl-2 level was significantly lower in diabetics than in non-diabetic subjects also serum Bcl-2 level was significantly lower in diabetics with vascular complications than in diabetics without vascular complications. There was a significant positive correlation between serum Bcl-2 level and serum urea, serum creatinine and proteinuria in diabetics with microvascular complications. On the other hand, a significant negative correlation was found between serum Bcl-2 level and glycated Hb% in diabetics with macrovascular complications.