Interestingly, overexpression of FOXO1, another member of the FOXO family of transcription factors, restored the expression of Fas-associated factor 1, prevented IRF3 nuclear translocation, and abrogated interferon-stimulated gene expression in human epithelial cells infected with T. gondii (53), suggesting a role for FOXO1 in the regulation of IFN-mediated responses during toxoplasmosis. The gene discussed is IRF3; the disease is toxoplasmosis.