This finding is supported by two reports about the relation between KMT2A and ETS1 in AML/MDS: both genes are coamplified and overexpressed [49], and the fusion KMT2A-EB1 (but not KMT2A-AF10) activates the expression of ETS1 [50]. The gene discussed is MLLT10; the disease is acute myeloid leukemia.