The loss of Hells was associated with reduced Dnmt3b binding to retroviral elements within the PU.1 gene suggesting that HELLS generally controls Dnmt3B binding to chromatin.120 The human HELLS homolog (also known as proliferation-associated SNF2-like gene product) is widely expressed in AML and ALL cell lines and primary samples. Here, DNMT3B is linked to acute myeloid leukemia.