CDK9 and glioblastoma: PRMT6 and CDK9 collaboratively influence the expression of YTHDF2, which in turn attaches to and accelerates the breakdown of antigen‐presenting cell (APC) and GSK3β, negative regulators of the WNT‐β‐catenin signalling cascade, thereby enhancing GBM migration, invasion and epithelial–mesenchymal transition (EMT), implying its suitability as a treatment target for GBM.71