We then investigated the changes in the Nrf2 pathway in the in vitro model of AD and found that Nrf2 expression and its intranuclear levels were significantly reduced in cells from the Aβ1−42-treated group compared to that in the control group, and overexpression of VILIP3 partially restored Nrf2 activity (Fig. 6f, g and Fig. S4c-e). This evidence concerns the gene HPCAL1 and Alzheimer disease.