The consensus on the mechanism of helminth therapy is essentially two-fold: Infection with parasitic helminths drives Th2-dominated immunity and this reduces disease caused by Th1 immunopathology, or mobilization of immunoregulatory cells/factors inhibits inflammation (e.g., Foxp3+ regulatory T cells (Tregs), alternatively activated macrophages (AAMs), IL-10, transforming growth factor β (TGFβ)) [21,26]. The gene discussed is TGFB1; the disease is infection.