For instance, in AD model rats, TGF-β1 pretreatment remarkably ameliorates amyloid-β (Aβ)1–42-induced neurodegeneration and prevents Aβ1–42-induced increases in glia-derived proinflammatory mediators and T cell-derived proinflammatory cytokines, in the hypothalamus, serum or cerebrospinal fluid (Chen et al., 2015). The gene discussed is TGFB1; the disease is Alzheimer disease.