NEAT1 and glioblastoma: HOTAIR functions as a scaffold for PRC2 and the LSD1/CoREST/REST complex as well as guiding these complexes to their endogenous targets and so activating pro‐oncogenic signalling pathways.93 HOTAIR regulates cell cycle progression in glioma cells via interaction with EZH2, and inhibition of HOTAIR represses GBM tumour growth in vivo.94 Additionally, PRC2 binding NEAT1 silencing in GBM cells was correlated with decreased H3K27me3 levels in PCGs as part of the Wnt/β‐catenin signalling pathway, such as Axin2.57