The role of apoptosis or programmed cell death in the pathophysiology of rheumatic diseases hab been an active area of research, and advances in the field were reviewed in a recent issue of Arthritis & Rlieurrintisrn (I). Defect5 in the regulation of apoptosis have been observed in both hematopoietic and nonhematopoietic tissues derived from patients with systemic lupus erythematosus (SLE), a dibcase characterized by immune abnormalities that allow the production of antinuclear antibodies directed against self antigens, particularly RNP complexes (23). In this review, we discuss the role of cell death in the generation of autoantibodies in patients with SLE and scleroderma, and wc present a unifying hypothesis to explain how defective apoptosis or ineffectivc clearance of apoptotic cells and modified autoantigens might contribute to the bypass of tolerance that is required for autoantibody formation.