Together, the authors point to an important mechanism through which IL-1β and IL-1R1 are related to Aβ accumulation, suggesting that therapeutics stimulating the TOM1 signaling pathway could be an appealing strategy to counteract the persistent activation of the IL-1/IL-1R1 complex, contributing to a homeostatic immune response in AD. This evidence concerns the gene IL1R1 and Alzheimer disease.