Here, we showed high expression of FoxP3 and GITR and their co-localization in the hippocampus of untreated 3xTg-AD mice while their expression was attenuated by treatment with the anti-TNFSF10 antibody, suggesting that neutralization of TNFSF10, known to increase the number and activity of Treg cells [16], achieves a significant anti-inflammatory effect. The gene discussed is TNFSF10; the disease is Alzheimer disease.