The Aβ peptide deposition‐induced formation of extracellular senile plaques is a hallmark of AD.[42] Accumulating evidence from genetic, biochemical, and animal model studies has strongly suggested that excessive Aβ accumulation plays a central role in AD pathogenesis.[43] In this study, we demonstrated that the absence of cGAS in microglia leads to a reduction in Aβ plaque load, suggesting that cGAS is involved in regulating the balance between Aβ accumulation and clearance. This evidence concerns the gene CGAS and Alzheimer disease.