CXCL1 and neoplasm: KAP1 depletion inhibited RIPK1 ubiquitination and reduced NF-κB-mediated CXCL1 release, thus limiting MDSC infiltration in syngeneic murine tumors.KAP1 overexpression caused bigger tumor sizes, higher MDSC infiltration, and decreased CD8+ T-cell presence in the TME. It conferred resistance to anti-PD-1 therapy.