This study investigates the role of branched N-glycans and fucosylation in ovarian cancers (EOCs) and their impact on immune checkpoint blockade (ICB) therapy. The research reveals that inhibiting branched N-glycans sensitizes HR-proficient EOCs to ICB, while fucosylation inhibition enhances anti-PD-L1 immunotherapy regardless of HR status. Mechanistically, BRCA1/2 transcriptionally upregulate MGMT, which catalyzes the formation of branched N-glycans. These glycans enhance PD-L1 binding to PD-1 on CD8+ T cells, reducing the effectiveness of anti-PD-L1 therapy. Inhibition of branched N-glycans using 2-Deoxy-D-glucose sensitizes HR-proficient EOCs to anti-PD-L1 in orthotopic mouse models, suggesting that targeting these glycans could be a promising therapeutic strategy for HR-proficient EOCs.This study investigates the role of branched N-glycans and fucosylation in ovarian cancers (EOCs) and their impact on immune checkpoint blockade (ICB) therapy. The research reveals that inhibiting branched N-glycans sensitizes HR-proficient EOCs to ICB, while fucosylation inhibition enhances anti-PD-L1 immunotherapy regardless of HR status. Mechanistically, BRCA1/2 transcriptionally upregulate MGMT, which catalyzes the formation of branched N-glycans. These glycans enhance PD-L1 binding to PD-1 on CD8+ T cells, reducing the effectiveness of anti-PD-L1 therapy. Inhibition of branched N-glycans using 2-Deoxy-D-glucose sensitizes HR-proficient EOCs to anti-PD-L1 in orthotopic mouse models, suggesting that targeting these glycans could be a promising therapeutic strategy for HR-proficient EOCs.