To get a more potent gene for cancer therapy, we have previously mutated the residues threonine 33 and serine 35 of Bik to aspartic acid to create the constitutively phosphorylated form, BikDD, with enhanced binding affinity to anti-apoptotic members Bcl-2, Bcl-Xl or Mcl-1 and greater pro-apoptotic activity [18]. This evidence concerns the gene BIK and cancer.