TP53 and neoplasm: The BFA’s novel mechanisms of chloride ion channel and membrane potential modulation may offer hope for a future adjunct treatment for these diseased cells.14 These tumor cells that retain their apoptotic programming appear to respond to the noted pro-apoptotic transcriptional upregulation but the cells that respond with autophagy may indeed be apoptotic (P53) deficient and therefore able to survive the current apoptosis inducing treatments.4,5 The BFA may lead to an oxidative stress that is prolonged enough for these cells to transition from survival to an irregular necrosis-like apoptosis.