The presence of mutations in genes encoding for activated signaling pathways (e.g., KIT and FLT3), or NPM1, chromatin–spliceosome complex, tumor suppressor genes (such as TP53 and WT1) and transcription factors (such as RUNX1 and CEBPA), and cohesion complex are increasingly recognized as important genetic alterations in AML (2). The gene discussed is FLT3; the disease is acute myeloid leukemia.