Thus, we explored BCL-2 RNA and protein expression after I-BET 151 treatment, as BCL-2 is a direct KMT2A target whose transcription is dependent on BET family protein placement on chromatin (Dawson et al., 2011), and we found that during treatment, BCL-2 was significantly decreased (Figures 2D,E, *p < 0.05, ***p < 0.001) in both RNA and protein expression, sensitizing KMT2A-AML to venetoclax treatment. Here, BCL2 is linked to acute myeloid leukemia.