Given the aggressive nature of H9M AML, its dependency on the sole overexpression of Hoxa9 and Meis1, and its anticipated genetic stability, the expansion of dedicated color codes suggests the acquisition of a limited number of H9M collaborating genetic aberrations or transcriptional adaptations with putative prognostic value for human AML [17,18]. The gene discussed is HOXA9; the disease is acute myeloid leukemia.