Apoptosis in HCT116 cells following anti-cancer drugs requires only Bax, but not Bak.58 This differential requirement has been attributed to the selective suppression of Bak by Mcl-1.59 However, it has also been suggested that the direct activator BH3-only proteins selectively activate Bax or Bak in response to chemotherapeutic agents.60 The creation of Bid/Bim/Puma TKO, Bid/Bim/Puma/p53 QKO, and PentaKO/Mcl-1−/− cells provides useful tools to help resolve the selectivity issue, which is critical in the apoptotic response in cancer following chemotherapeutic treatments. Here, BAK1 is linked to cancer.