miR-625 was found to bind to IGF2BP1 and inhibit tumor migration and invasion, which may have partly resulted from the speculated IGF2BP1/PTEN/HSP27 pathway in which the re-expression of miR-625 might indirectly reduce PTEN expression through depressing IGF2BP1, subsequently contributing to the Akt-mediated phosphorylation of HSP27 and suppressing F-actin polymerization [42]. The gene discussed is IGF2BP1; the disease is neoplasm.