As suggested by the global sensitivity analysis (figure 10), effector T-cell apoptosis, induced by IL-10 secretion from MDSCs and tumour cells, inhibition of cytotoxic activity of effector T cells through arginase or NO production by MDSCs that do not require antigen-specific interactions, and Treg induction and expansion by IL-10 and TGF-β may also contribute to the immunosuppressive TME in breast cancer patients [60–62]. The gene discussed is IL10; the disease is neoplasm.