As Th1, Th2, and Th17 responses are involved in the pathogenesis of AD,8,10,14 oral administration of KBL382 modulated the adaptive immune response, leading to suppression of Th1 (IL-2 and IFN-γ), Th2 (IL-4, IL-5, IL-13, and IL-31), and Th17 (IL-17A) cytokines (Figure 5A-E, G-H, and S2C-E). The gene discussed is IFNG; the disease is Alzheimer disease.