Recently, an experiment investigating CXCR3 antagonists in the amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic mouse model of AD showed that CXCR3 antagonists increased Aβ phagocytosis in microglia and ameliorated behavioral deficits in diseased mice, suggesting that CXCR3 axis mediates AD‐like pathology in APP/PS1 mice and could be a therapeutic candidate for AD.334. The gene discussed is APP; the disease is Alzheimer disease.