Neuroinflammation, with its associated elevation of interleukin-1 (IL-1) α and β synthesis and release, and autophagic failure, with its associated buildup of ubiquitinated protein aggregates in autophagosomes, are now recognized as early events in the Alzheimer-related neuropathogenesis of Down’s syndrome [1–4] and, analoguously, of early events in the neuropathogenesis of Alzheimer’s disease (AD) [3, 5, 6]. The gene discussed is IL1B; the disease is Down syndrome.