In an SR-A-deficient mouse model of AD, microglia-mediated phagocytosis of soluble Aβ was reduced, and the expression levels of enkephalinase and insulin-like growth factor 1 (IGF-1), which have been reported to be Aβ-degrading enzymes in AD, were also significantly reduced, suggesting that SR-A may alleviate AD by affecting Aβ phagocytosis (95). The gene discussed is IGF1; the disease is Alzheimer disease.