Together, these findings suggest that AML1‐ETO in an abnormal chromatin remodelling complex with other cofactors (e.g. DNMTs) mediates hypermethylation of CpG islands around AML1‐binding sites on the THAP10 promoter, while probably increasing histone deacetylation (e.g. by HDAC1) on the THAP10 promoter as well, which might represent a novel mechanism responsible for suppression of THAP10 expression in t(8;21) AML. Here, HDAC1 is linked to acute myeloid leukemia.