Apoptosis was first described in 1972 by Kerr et al. Apoptosis has been applied to a form of cellular death also known as “programmed cell death” or cell suicide. Recent studies have shown that apoptosis is involved in pathophysiologic changes seen in various renal diseases. Alteration in apoptosis related genes such as Fas-Ligands results in autoimmune disease and renal damage. A main function attributed to B cell leukemia/lymphoma 2 gene (bcl-2) is its ability to confer resistance against apoptosis.All patients had their serum Bcl-2 estimated. Also we compared the serum Bcl-2 results between the untreated cases with FSGS and the group who started the treatment. The disease parameters include the rise of blood pressure, degree of proteinuria and rise of serum creatinine. There is a significant decline of mean serum Bcl-2 in our untreated adults and children cases with FSGS compared to the normal controls while serum Fas-ligands significantly rise in this group. This indicates an enhanced state of apoptosis with increase pro-apoptosis and reduced anti-apoptosis. Bcl-2 may have been localized in regenerating tubular cells within atrophic tubules. Increased levels of renal Bcl-2 mRNA and protein have been described in regenerating tubular cells after an ischemic injury. Finally, the Bcl-2 antiapoptotic influence is modulated by other members of its family, including Bcl-xL. Sato et al described significant rise in serum levels of sFas and Fas-L in the peripheral blood of patients with various renal diseases.FSGS represents a unique feature among different forms of GN where enhanced apoptosis plays an important pathogenic role in inducing the sclerotic lesion and blocking this enhanced apoptosis early in the disease may be of a crucial prognostic value.