AKR1B1 promoted breast cancer progression by activation of EMT.32 MT2A played a tumour suppressor role through inhibiting NF‐κB signalling and was a prognostic biomarker for tumour patients.33 UBC was regarded as a promising therapeutic target for ovarian cancer patients with recurrent UBB silencing.34 Noticeably, both our data and the CCLE database showed the overexpression of AKR1B1, MT2A and UBC in GBM cells (Figure 2A and Figure S3), implying that these genes might play oncogenic roles in GBM cells. This evidence concerns the gene UBC and glioblastoma.