The anti-inflammatory effect of these drugs gives another explanation for the inhibited PS1/BACE-1/Aβ axis where the inflammatory cascade was recounted to activate the PS1/BACE-1/Aβ hub (Paouri et al., 2017) and to increase the formation of ROS, which in turn elevates also the AD-related markers (Kummer and Heneka, 2008; He et al., 2017). The gene discussed is BACE1; the disease is Alzheimer disease.