RNASET2 and neoplasm: Of note, in the in vivo C51-based syngeneic model, a strong Rnaset2-dependent retardation in tumor growth rate was observed, concomitant with early tumor infiltration by M1 macrophages, inhibition of M2 and myeloid-derived suppressor cells (MDSCs) cells and, very interestingly, a later expansion of CD8+ T lymphocytes with rejection capacity and antitumor recall immunity [50].