Our results above demonstrated that inhibition of USP8 by genetic depletion or the pharmacological inhibitor, DUBs-IN-2, dramatically upregulates PD-L1 protein levels as well as multiple innate and adaptive immune response signaling pathways that might reshape an inflamed TME to enhance anti-tumor immunity (Figs. 1, 4, and 5). The gene discussed is USP8; the disease is neoplasm.