Targeting either CEBPB or S100A8 could overcome ICB resistance and remodel the tumor microenvironment.<h4>Conclusions</h4>Our study demonstrate a mechanistic link between tumor dormancy and immune evasion, highlighting the CEBPB-S100A8 axis as a promising therapeutic target to potentiate ICB efficacy in TNBC. Here, S100A8 is linked to neoplasm.