Thus, it seemed plausible that a full-length BIM or a BH3 region bearing the I155R and E158S substitutions could be phosphorylated in cancer cells with elevated Akt activity and then be converted into a potent inhibitor against antiapoptotic BCL-2 proteins, while they are not potentiated in normal cells due to low or controlled Akt activity. Here, BCL2L11 is linked to cancer.