For example, although maraviroc binds to CCR5 to block interaction between HIV-1 and CCR5 and prevent HIV-1 entry into host T cells and macrophages51, recent studies have shown that it also blocks interactions between cancer cells and immune and other cells in the tumor microenvironment56, reprograms immunosuppressive myeloid cells, and enhances antitumor immunity by targeting an autocrine CCL5-CCR5 axis in BM57. Here, CCL5 is linked to neoplasm.