In addition, USP5 depletion in tumor cells upregulated the expression of costimulator CD86 and antigen-presentation molecule HLA-DR on cocultured THP1-MΦ (Figure 4D), and the CD40 protein of murine RAW264.7 macrophages was also upregulated after coculture with IFN-β–treated Usp5-KO CT26 cells (Figure 4E), confirming that depletion of tumor-intrinsic USP5 could induce IFN-I–responsive CXCL9hi macrophages and augment their immune-activating capacity. The gene discussed is CD86; the disease is neoplasm.