demonstrated that MLL-fusion/MYC⊣miR-26a⊣TET1 signaling circuit played an important role in AML, in which hsa-mir-26a-5p functioned as an essential tumor-suppressor mediator and its transcriptional repression was required for the overexpression and oncogenic function of TET1 in MLL-rearranged AML (42). The gene discussed is KMT2A; the disease is neoplasm.