The findings of our study, demonstrating that N-glycosylation of PD-L1 at all four sites interferes with the blocking activities of ICBs directed to PD-L1 or PD-1, suggest that patients whose tumors have low N-glycosylation levels would potentially respond better to such ICBs than patients whose cancer express high N-glycosylation levels. The gene discussed is PDCD1; the disease is cancer.