Although only the addition of the BCL-XL-selective inhibitor a-1331852 has been found to be effective in overcoming resistance related to the SWI-SNF complex mutations in MCL (39), the initiation phase of the mechanism, such as chromatin remodeling, could be targeted, such as the addition of chromatin remodeling-related drugs to venetoclax [e.g., vorinostat and panobinostat (histone deacetylase inhibitors)], a clinical trial of vorinostat in combination with venetoclax in AML is currently underway (NCT05317403). Here, BCL2L1 is linked to acute myeloid leukemia.