In fact, a large body of work in experimental animal models of infection, inflammation, and cancer suggests that major immune effector cytokines, including IL-6, IL-1, type I and II IFNs, IL-23, and IL-4, can cause Treg cells to lose Foxp3 expression, become functionally inactivated, and acquire pro-inflammatory features, or render immune effector cells refractory to Treg cell-mediated suppression14, 15, 16, 17, 18, 19, 20. The gene discussed is FOXP3; the disease is infection.