IL-10, in combination with TGF-β, seems to be powerful enough to completely suppress the gene expression of inflammatory mediators in the brain after 14 days of infection, but this is not an endless control, as reported also in a stroke model using IL-10 knockout mice, where IL-10 play a role in attenuation, but not in resolution of neuroinflammation57. The gene discussed is TGFB1; the disease is infection.