This phenomenon was also pronounced for GCNT2 methylation in AML, where patients with WT1 mutation were enriched in hypermethylation of GCNT2 isoform A. In our Binary logistic regression model, age, inv (16), t (15;17), genes mutations of DNMT3A, CEBPA, RUNX1, and WT1 were deemed to independently correlate with methylation of GCNT2 isoform A, suggesting that the diverse phenotypic features of AML, which were attributed by distinctive cytogenetic or molecular abnormalities, came in the way of regulating GCNT2 methylation. This evidence concerns the gene GCNT2 and acute myeloid leukemia.