RUNX1 and acute myeloid leukemia: Upregulation of genes normally expressed in hematopoietic progenitor cells or lymphoid cells, and downregulation of promoters of myelopoeisis also ascribe a unique gene expression signature to RUNX1-mutated AML [3,12], implicating upregulation of oncogenic pathways such as BCR, TLR-4 and NOTCH1 to the pathogenicity of mutant RUNX1.