To determine the cell population responsible for cGAS elevation in AD, we treated 5xFAD mice with CSF1R inhibitor PLX5622, a compound known to selectively deplete microglia.[27] In line with the induction of cGAS signaling observed in human AD, both cGAS and STING protein levels were significantly induced in 5xFAD mice compared to age‐matched wild‐type controls (Figure 1c). The gene discussed is CGAS; the disease is Alzheimer disease.