The CCR5/CCL5 signaling axis has been shown to increase infiltration of regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) into the tumor microenvironment (TME), creating an immune effector cell desert that promotes cancer survival and progression (Sevimoglu and Arga, 2014), while potentially contributing to immunotherapy resistance. The gene discussed is CCR5; the disease is neoplasm.