Moreover, mutated Bcl-w and Bcl-XL proteins that do not bind to Bax (i.e., Bcl-wG94A and Bcl-XLG138A) fail to stimulate ROS production, cell invasion [22], and cancer cell intravasation in mouse models [25], supporting the notion that pro-survival Bcl-2 family members promote ROS production, cell invasion, and cancer metastasis by binding to multidomain pro-apoptotic members and blocking their inhibitory effects on ROS production. This evidence concerns the gene BCL2L1 and cancer.