According to our results, N2a-wt cells expressed higher levels of Hmox1 than N2a-APP overexpressing cells, which corroborates data from the literature reporting that the ROS-dependent mechanism of activating the Nrf2/ARE pathway has become unresponsive in AD models [31] and that AD patients have a decrease in nuclear Nrf2 levels [4]. The gene discussed is HMOX1; the disease is Alzheimer disease.