In conclusion, through our comprehensive in silico analysis, we showed that overexpression and a strong positive correlation of the CDK1/PBK/CHEK1 oncogenic signature in GBM promote its aggressiveness, immuno-evasion, and tumor progression through an aberrant completion of the cell cycle and recruitment of the tumor-promoting immune cells such as the T Cells CD4+ Th2 subtype, MDSCs, and the TAM-M2 subtype. This evidence concerns the gene PBK and neoplasm.