In silico stratification analyses of molecular data from AML patients revealed a reciprocal relationship between MYB and MAFB expression, highlighting a novel biological interconnection between these two factors in AML and supporting new rationales for targeting MAFB in MLL‐rearranged leukemia.[36] MAFB has been reported to promote cancer stemness and tumorigenesis in osteosarcoma through a Sox9‐mediated positive feedback loop.[37] These results suggest that our model can effectively capture drug response biomarkers for AML. The gene discussed is KMT2A; the disease is acute myeloid leukemia.