Thus, the present study provides experimental evidence and clinical data supporting the hypotheses that: i) miRNA can be methylated at cytosine residues by DNMT3A/AGO4-including complexes; ii) the presence of 5-methylcytosine (5mC) in miRNA abolishes their repressive function towards the gene expression; and iii) miRNA methylation is associated with poor prognosis in glioma (Fig. 6). Here, DNMT3A is linked to glioma.