Model for regulation of oncogene-driven apoptosis by BCL-2 family proteins. Oncogenic stress pathways lead to activation of several BH3-only proteins. They all antagonize pro-survival BCL-2 members but in addition certain of these BH3-only members also activate BAX and BAK. When in excess, pro-survival members prevent apoptosis by antagonizing the activated conformers of BAX and BAK. Therapeutics that shift the balance in favor of excess antagonists of pro-survival members should permit oncogenic stress pathways to productively engage the apoptosis mechanism. Details are given in the text.