Understanding the mechanism by which FoxP3 expression regulates the immune process in AE could help find new immunotherapeutic targets, since the metacestode disappearance we observed by depleting FoxP3 Treg cells in hosts with fully established metacestode was never equaled with other types of immune manipulation; up to now, only pre‐infection administration of IL‐12 was able to effectively suppress AE occurrence in the mouse model; as this was not applicable to humans, it was never tested as a therapeutic agent 23. This evidence concerns the gene FOXP3 and infection.