Ma et al. (2016) found that the knockdown of the lncRNA NEAT2 in gliomas could result in the significantly increased permeability of BTB, which might contribute to enhancing potential therapeutic strategies for human gliomas. Meanwhile, the results from Liu’s group indicated that the lncRNA TUG1, which is highly expressed in vascular endothelial cells from glioma tissues, could influence BTB permeability via binding to miR-144, further reducing the expression of tight junction proteins in endothelial cells, such as ZO-1, occludin, and claudin-5 (Cai et al., 2015). This evidence concerns the gene MALAT1 and glioma.