RUNX1 and acute myeloid leukemia: A two-hit model proposes that the development of AML requires cooperation between at least two classes of gene mutations; Class I mutations, such as FLT3, RAS, JAK2, PTPN11, and KIT mutations activate genes in the kinase signalling pathways conferring proliferation and/or survival advantage to haematopoietic cells and Class II mutations, such as RUNX1/RUNX1T1, PML/RARα, CBFB/MYH11, MLL/PTD, AML1/RUNX1, and CEBPA mutations, affect transcription factors impairing haematopoietic differentiation (Gilliland, 2002; McCormack et al, 2008; Renneville et al, 2008).