In murine models of Alzheimer's disease and Parkinson's disease, REAC protocols have been shown to modulate pathological neuroinflammation, downregulating pro-inflammatory mediators such as interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and inducible nitric oxide synthase (iNOS), while upregulating anti-inflammatory factors including interleukin-10 (IL-10) and suppressor of cytokine signaling-1 (SOCS-1) [19]. The gene discussed is IL1B; the disease is early-onset autosomal dominant Alzheimer disease.