Other studies have shown that higher levels of H3K79me2 are associated with poorer prognosis in MLL-r leukemias [63], and the fusion of DOT1L and MLL partners, AF4, AF9, ENL, and AF10, leads to misregulation of DOT1L targets, resulting in aberrant H3K79me2 activity followed by leukemic transformation [64, 65]. The gene discussed is AFF1; the disease is leukemia.