Often, AML arises through the collaboration between mutations affecting transcription factors (e.g., CEBPA, PU.1, and RUNX1) and signalling proteins (such as FLT3, RAS, and KIT) that lead to an aberrant proliferation capacity coupled with a disruption of terminal myeloid differentiation (Tenen, 2003; Rosenbauer & Tenen, 2007). This evidence concerns the gene FLT3 and acute myeloid leukemia.