Although RUNX1 mutation was reported to promote hypermethylation in AML (56), however, we observed that RUNX1 mutation was associated with GCNT2 hypomethylation, assuming that guiding DNMT3A to the binding site by RUNX1 and leading to GCNT2 methylation was blocked by the mutation in RUNX1. Another piece of evidence is that the RUNX1-RUNX1T1 fusion protein stemming from t (8;21) retained the binding site of RUNX1 which promoted methylation of target genes in AML (50, 62). Here, GCNT2 is linked to acute myeloid leukemia.