There has been a significant progress in understanding the biology of AML including identification of translocations leading to aberrant fusion proteins such as t(8:21) (q22;q22), inv(16) (p13.1q22), t(9;11) (p21.3;q23.3), t(15;17) (q22;q12), t(9;11) (p22;q23), or gene-specific somatic mutations in Fms-like tyrosine kinase (FLT3), IDH1/2, P53, CEBPA, NPM1, DNMT3A, c-KIT, TET2, MLL, and others. The gene discussed is DNMT3A; the disease is acute myeloid leukemia.