While most large-scale cohort studies report that increased Cdk5 expression is associated with tumor progression and poor clinical outcomes [110,115], recent immune studies have revealed a paradoxical, tumor-suppressive role where Cdk5 promotes the autophagic degradation of the immune checkpoint molecule programmed death-ligand 1 (PD-L1), thereby potentially enhancing anti-tumor immunity [126]. The gene discussed is CDK5; the disease is neoplasm.