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). The gene discussed is CD68; the disease is Alzheimer disease.