Therefore, in contrast to the reported miR-22 oncogenic function and overexpression in MDS, they showed that miR-22 has an antitumor effect in the pathogenesis of AML, and it is significantly downregulated in most de novo AML patients due to TET1/GFI1/EZH2/SIN3A-mediated epigenetic repression and/or DNA copy number loss. The gene discussed is SIN3A; the disease is acute myeloid leukemia.