Menin and Bcl-2 inhibition targets leukemia and stem/progenitor cells, modulates Bcl-2 protein levels in BM cells, and exhibits enhanced antileukemia activity in primary AML patient samples. Cell populations were PhenoGraph clustered based on cell surface markers. Cisplatin-low viable single cells were gated with FlowJo software v10.7 and exported as flow cytometry standard data for subsequent analysis in Cytofkit.²⁵ Cell populations identified and embedded by PhenoGraph in the “Cytofkit_analyzedFCS” files were gated in FlowJo to quantify marker expression. ArcSinh-transformed counts for each protein expression in desired cell populations were visualized using heat maps. (A) huCD45⁺ cells in various treatment groups. (B) Clusters of leukemia cells and leukemia stem/progenitor cells. (C) Percentage of viable leukemia cells and leukemia stem/progenitor cells in each treatment group. (D) Protein expression in huCD45⁺ cells in various treatment groups. (E) Percentage of huCD11b⁺CD45⁺ cells in each treatment group. (F) Mononuclear cells from NPM1/FLT3-mutant AML patient samples (n = 5) were treated with SNDX-50469, venetoclax, or both for 24 hours. Apoptosis, cell viability, and p-FLT3 levels were determined by flow cytometry. Samples were obtained after acquiring written informed consent following the MD Anderson Cancer Center Institutional Review Board–approved protocol and in accordance with the Declaration of Helsinki. Differences between groups were determined using the Student t test. Values of P ≤.05 were considered statistically significant. con/CON, control; SNDX, SNDX-50469; VEN, venetoclax.