Recent studies suggested that in acute myeloid leukemia (AML) cells, mutated FMS-like tyrosine kinase 3 with internal tandem duplications (FLT3-ITDs) increases the synthesis of transcription factor signal transducer and activator of transcription 5 (STAT5), which binds to the NOX4 promoter region at IFN-γ activated sequence elements, activating NOX4 gene transcription. The gene discussed is IFNG; the disease is acute myeloid leukemia.