Furthermore, it shows a greater affinity for BCL-2 than for BCL-W or BCL-XL, giving it a predominance over the ABT-737 and navitoclax (ABT-263) molecules, which both bind to BCL-W and BCL-XL, also present on platelets, thereby causing thrombocytopenia, which limits their clinical usefulness [52,55]. This evidence concerns the gene BCL2L1 and Thrombocytopenia.