In T-cell ALL (T-ALL) and MLL-rearranged (MLL-r) ALL, METTL16 was shown to stimulate the production of MAT2A mRNA encoding methionine adenosyltransferase 2A (MAT2A, the SAM synthase) by promoting the splicing of an intron, which afterward enables the functions of multiple methyltransferases, including DOT1L and PRMT5 (Pendleton et al. 2017; Secker et al. 2020), thereby provoking pathogenesis. Here, DOT1L is linked to acute lymphoblastic leukemia.