Investigation of the role of the RAS in the MM TME by Nakamura et al. (174) demonstrates that fibroblasts produce CC motif chemokine ligand 5 (CCL5) upon stimulation of the RAS, which is suppressed upon ARB administration in mice, and that ARB administration (1) decreases CCL5 blood concentration, (2) increases tumor-infiltrating T cells, (3) decreases regulatory T cells, and (4) increases tumor antigen-specific T-cell responses. Here, CCL5 is linked to neoplasm.