Regardless of the interconnected hierarchical model explaining how the BCL-2 family proteins dictate cellular survival versus mitochondrion-dependent cell death [72–76], we now provide solid evidence that intrinsic/primary unresponsiveness of cancer cells to BCL2-targeting BH3 mimetics can be circumvented by promoting a high mitochondrial primed-for-death state with FASNis. This evidence concerns the gene BCL2 and cancer.