Consequently, FPR1/FPRL1 and RAGE or MARCO interactions may explain how formyl peptide receptors interact with a menagerie of structurally diverse pro- and anti-inflammatory ligands associated with different diseases including amyloidosis, Alzheimer’s disease, prion disease and HIV, or with bacterial components[14,21]. The gene discussed is FPR1; the disease is early-onset autosomal dominant Alzheimer disease.