To investigate whether combination drug therapy could potentiate NFκB inactivation, we conducted a synthetic-lethal chemical screen intended to reveal novel targets in aRMS tumors with deleted IKKβ. Five of 6 tested aRMS tumor cell samples exhibited sensitivity to the BCL-2 inhibitor navitoclax (Fig. 3A), an orally bioavailable small-molecule protein inhibitor that is currently in Phase 1 trials for recurrent non-small-cell lung carcinoma and recurrent hepatocellular carcinoma, and Phase 2 clinical trials for platinum resistant/refractory ovarian cancer. This evidence concerns the gene NFKB1 and neoplasm.