Direct fusion of DOT1L to MLL was sufficient to activate transcription of HOXAs. 39 Loss of DOT1L resulted in reduction of cell growth, increased differentiation and apoptosis of MLL-AF9 leukaemic cells, indicating its potential as a target for AML therapy.38 On the other hand, PRMT1 is the founding member of PRMTs that mediates arginine methylation on both histone (H4R3me2a) and non-histone substrates (for example, transcription factors and splicing factors). The gene discussed is DOT1L; the disease is acute myeloid leukemia.