The Bcl-2 gene was isolated at the chromosomal breakpoint of t-bearing follicular B cell lymphomas. Bcl-2 blocks cell death following a variety of stimuli and confers a death-sparing effect to certain hematopoietic cell lines following growth factor withdrawal. Bcl-2 is localized to outer mitochondrial membranes and endoplasmic reticulum as well as nuclear membranes. A related protein, designated Bax p21 (for Bcl-associated X protein), has extensive amino acid homology with Bcl-2 and both homodimerizes and forms heterodimers with Bcl-2. Overexpression of Bax accelerates apoptotic death induced by cytokine deprivation in an IL-3 dependent cell line, and Bax also counters the death repressor activity of Bcl-2.