In a transgenic model of AD, administration of an amylin antagonist reduced inflammatory microglial markers, including ionized calcium binding adaptor molecule 1 (Iba1) and CD68, caspase-1, TNFα, and IL1β, and a concordant reduction in Aβ plaque burden and size compared to controls, implicating amylin in the pathogenesis of AD (Fu et al., 2017). This evidence concerns the gene TNF and Alzheimer disease.