NFKB1 and glioblastoma: Glioblastoma cell studies have revealed that elevated HK2 expression under high glucose conditions promotes the phosphorylation of inhibitory protein IκBα within nuclear factor κB (NF-κB), leading to IκBα degradation and a subsequent NF-kB activation–dependent increase in PD-L1 expression, facilitating immune evasion [19].