The selectivity of venetoclax for BCL2 was an advance on the therapeutic index of its predecessor, navitoclax (ABT-263), whose demonstrated efficacy in R/R CLL was compromised by dose limiting thrombocytopenia due to on target inhibition of another BCL2 family protein, B-cell lymphoma-extra large (BCL-XL), which controls physiologic platelet lifespan[32,37]. This evidence concerns the gene BCL2 and B-cell chronic lymphocytic leukemia.