RUNX1 and acute myeloid leukemia: Type I abnormalities result in increased, uncontrolled proliferation and/or survival of the leukemic cell and are often activating mutations of genes involved in signal transduction pathways, such as FLT3, KIT, N-RAS, K-RAS and PTPN11. Type II abnormalities impair differentiation and mainly result from genetic aberrations in hematopoietic transcription factors, due to, for instance, the AML-characteristic translocations t(8;21)(q22;q22)/AML1-ETO and 11q23/MLL rearrangements or from mutations in genes, such as NPM1 and CEBPA [7,45,46,47,48].