Treatment with navitoclax (or ABT-263, a BH3 mimetic that inhibits the anti-apoptotic factors BCL-xL and BCL-2) to enhance “free” cellular BIM levels or derepression of BIM expression by depletion of ZEB1 both led to resensitization of mesenchymal EGFR-mutant cancers to targeted therapy. This evidence concerns the gene BCL2L11 and cancer.