As the major reader of m6A, YTHDF2 has been reported to promote malignancy of gliomas through facilitating mRNA decay of UBXN1 and subsequent activation of NF-kB.30 In addition, YTHDF2 was found to cooperate with METTL3 and promoted HCC progression by destabilizing mRNA of SOCS2.31 Previous studies have mostly focused on the role of YTHDF2 in mediating mRNA metabolism and tumor progression through m6A methylation; however, the specific functional regulation of YTHDF2, especially post-translational modification, remains largely unexplored. Here, SOCS2 is linked to glioma.