This is further supported by the similar trends in OS between IDH wild-type LGG and GBM.2 In terms of the relevant therapeutic implication, previous work has also shown that depletion of HK2 but not HK1 restores oxidative phosphorylation and sensitizes GBM cells to standard therapy.57 Thus, in addition to LDHA, HK2 may serve as a potential candidate target for follow-up experimental studies that explore dual inhibition of the immunometabolic interface in glioma. This evidence concerns the gene HK1 and glioblastoma.