As plasma exposures of navitoclax in patients treated with this agent (Gandhi et al, 2011) are considerably higher than those achieved with obatoclax (O’Brien et al, 2009) due to CNS-limiting events, one explanation for the low rate of thrombocytopenia seen with obatoclax may be that obatoclax does not achieve the concentrations in platelets necessary to completely inhibit BCL-XL. This evidence concerns the gene BCL2L1 and Thrombocytopenia.