This notable and strict conservation of AF10OMLZ and therefore the DOT1L-binding capability in all leukemia-associated AF10 fusions suggests a likely mechanism underlying the development of AF10-rearranged leukemias that involves the aberrant recruitment and/or stabilization of DOT1L at promoters of leukemogenic genes and constitutive activation of these genes. Here, MLLT10 is linked to leukemia.