NFE2L1 and glioma: Given that CD38 is recognized as a promising therapeutic target in glioma treatment [29], and that NFE2L1 suppression heightened glioma responsiveness to anti‐PD1, we hypothesized that a synergistic approach involving anti‐PD1 monoclonal antibodies (mAbs) and CD38 inhibitors could potently suppress glioma progression.