For example, Chen et al. found that pseudogene PRELID1P6 was over-expressed in glioma and promoted glioma progression by affecting the cellular localization of hnRNPH1, thereby protecting hnRNPH1 from ubiquitin-mediated degradation which led to up-regulated TRF2 expression and activated the Akt/mTOR pathway (Xi et al., 2021). This evidence concerns the gene AKT1 and central nervous system cancer.