USP15 negatively regulates the activation of naive CD4+ T-cells and the generation of IFNγ, as well as the redundancy of IFNγ in USP15-deficient mice, which increases the expression of programmed death ligand 1 (PD-L1) and the C-X-C motif chemokine ligand 12 (CXCL12) to promote the immunosuppressive tumor microenvironment processed by immunosuppressive tumors induced by methylcholantrene [114]. The gene discussed is IFNG; the disease is neoplasm.