Various mechanisms can account for MYC overexpression in AML, including trisomy 8 resulting in single copy gain of MYC, MYC amplification, and deregulated expression due to an upstream mutation (for example in FLT3, a gene encoding a receptor tyrosine kinase); 9 % of AMLs are characterized by trisomy 8, making it the most common chromosomal abnormality in human AML [13]. The gene discussed is FLT3; the disease is acute myeloid leukemia.