Specifically, in human glioblastoma cells, high glucose levels promote the dissociation of hexokinase 2 (HK2) from mitochondria, subsequently mediating phosphorylation at the IκBα T291 site and promoting IκBα degradation, thus activating the NF-κB pathway and upregulating PD-L1 expression at the transcriptional level. Here, NFKBIA is linked to glioblastoma.