The marked increases in patient responses to venetoclax compared to navitoclax across BCL-2-dependent malignancies—for instance, 79% for venetoclax [12] and 35% for navitoclax [33] in CLL—underline that navitoclax, limited by thrombocytopenia, was insufficient to robustly inhibit BCL-2 in patients. This evidence concerns the gene BCL2 and Thrombocytopenia.