Moreover, detailed subclonal analyses that dissect whether MCL-1, BCL-XL, or other anti-apoptotic factors eventually supplant BCL-2 might clarify how MDS cells escape monotherapy and which rational combination regimens (e.g., dual BCL-2/MCL-1 inhibitors, BCL-2 + FLT3 blockade, or BCL-2 + PD-1/PD-L1 immunotherapy approaches) could lead to more durable remissions [26,29]. This evidence concerns the gene BCL2L1 and myelodysplastic syndrome.