For instance, IFNγ is known to promote NADPH oxidase 1 (NOX1) or NADPH oxidase2 (NOX2)‐mediated oxidative stress in microglia as well as activate signal transducer and activator of transcription 1 (STAT1) and NFκB followed by iNOS signaling pathways.[34] In this study, we for the first time revealed that IFNγ promoted the accumulation of oxidative stress in microglia under AD conditions by Keap1‐mediated Nrf2 downregulation (Figure 3g–j) leading to the reduction of antioxidant enzyme as the Catalase (Figure 3k). The gene discussed is CYBB; the disease is Alzheimer disease.