Chang et al. [48] found that METLL3 was significantly overexpressed in IDH-wildtype GBMs, and METLL3 enhanced the stability of long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) through m6A modification with the help of human antigen R (HuR) and activated nuclear factor-κB (NF-κB) pathway to promote malignant progression of IDH-wildtype gliomas. This evidence concerns the gene MALAT1 and glioma.