They found that the depletion of PMN-MDSCs decreases the growth of cisplatin-resistant tumor in mice by enhancing the infiltration of the CD8+ T cells; in turn, this depletion increases anti-PD-L1 immunotherapy, suggesting the promising benefit of the combinatorial treatment of anti-PD-1/PD-L1 and PMN-MDSC-incapacitating therapy in urothelial tumor patients. The gene discussed is CD8A; the disease is neoplasm.