As global knockout of IL-10 will have many off target effects that are not directly related to fluoxetine, we also used an α-IL-10R antibody and found that blocking IL-10 signaling during infection did not result in any significant differences in susceptibility of vehicle-pretreated mice to sepsis but did abolish the protective effects of fluoxetine, similar to what we observed with Il10−/− mice. The gene discussed is IL10RA; the disease is infection.