The bioinformatics and biological approaches of Wang’s study have demonstrated that the tumor-suppressive PRDM1 was a direct target gene of miR-30a-5p, and aberrant deficiency of PRDM1 was attributable to miR-30a-5p overexpression in GBM which contribute to phenotype maintenance and pathogenesis of gliomas [15]. This evidence concerns the gene PRDM1 and glioma.