While MIR376A was downregulated in esophageal cancer [35] and melanomas [36] and upregulated in salivary gland adenomas,[37] and pancreatic carcinomas,[38], [39]MIR376B was differentially expressed in uterine leiomyomas [40] and renal cell carcinomas.[41] Moreover, changes in MIR376A levels could be used as a marker to distinguish acute myeloid leukemia subtypes, but MIR376B could serve as a breast cancer subtype marker.[42] Additionally, MIR376A and MIR376B were subjected to variable levels of editing in glioblastomas.[43]. This evidence concerns the gene MIR376B and acute myeloid leukemia.