Expression of MCL-1 at the protein level does not directly correlate with resistance to navitoclax or venetoclax in NHL cell lines herein, or at the gene level with ABT-737 in chronic lymphocytic leukemia.24 Treatment of resistant NHL cell lines with navitoclax, venetoclax or A-1155463 resulted in enhanced MCL-1:BIM interactions that we hypothesized to inhibit BAX/BAK activation and subsequently limit the efficacy of these compounds. This evidence concerns the gene BCL2L11 and B-cell chronic lymphocytic leukemia.