These results provide the rationale for developing drugs to either selectively deplete deleterious tumor-specific CD4 + FoxP3 + T-cells, or to reposition certain agonistic oncology drugs (e.g. anti-OX40) in the field of autoimmune diseases and transplantation, should they indeed boost CD4 + FoxP3 + Treg-cells. This evidence concerns the gene TNFRSF4 and autoimmune disease.