Nevertheless, in pathological process such as AD, TGFβ could promote astrocyte reactivity, up-regulate IFITM3 expression, activate γ-secretase and promote Aβ accumulation through TGFBRI/Smad signal pathway [39, 40, 64], suggesting that astrocytes could be activated by TGFβ with the assistance of ENG. This evidence concerns the gene TGFB1 and Alzheimer disease.