It has also been suggested that FPRs mediate the uptake and fibril formation of amyloid-β in AD; transient FPR2/ALX activation in macrophages by amyloid-β stimulates rapid internalisation and degradation of the protein, however chronic stimulation leads to a build-up of amyloid-β-FPR complexes leading to the formation of fibrillar aggregates [22]. The gene discussed is FPR2; the disease is Alzheimer disease.