A ‘two-hit’ model has been widely accepted for AML pathogenesis27, in which full-blown and more aggressive AMLs are frequently caused by combinatorial genetic mutations, with one perturbing hematopoietic cell self-renewal or differentiation (often a mutation of a transcription/epigenetic factor gene) and the other promoting proliferation (often a mutation of a Receptor Tyrosine Kinase [RTK] signal transduction-related protein). The gene discussed is NTRK1; the disease is acute myeloid leukemia.