Based on the differential sensitivity of these antiapoptotic genes to splicing modulator E7107, and because of the cooperative role of BCL2 family members in supporting cancer cell survival, we then pursued these therapeutic hypotheses: (1) E7107 may induce cytotoxicity preferentially in cancer cells with MCL1 or BCL2A1 dependency by splicing perturbation of these genes; and (2) E7107 may synergize with inhibitors of BCLxL (encoded by BCL2L1), whose splicing is insensitive to E7107, to potentiate the cytotoxicity in cancer cells. Here, MCL1 is linked to cancer.