A recent study reported neuronal calmodulin-dependent kinase kinase-2 (CaMKK2) as a driver for the resistance to ICIs in glioblastoma[56], in which CaMKK2 increased CD8 T cell exhaustion, reduced CD4 effector cell expansion, and played a role in the maintenance of immunosuppressive phenotype of tumor-associated microglia[135]. Here, CD4 is linked to neoplasm.