In 2005, Singer and colleagues aimed at targeting BACE1, a protein involved in the processing of APP into amyloid, and by infusion of lentiviral vectors expressing shRNA targeting BACE1 into a transgenic AD mouse model they showed decreased levels of both APP and amyloid β, which was accompanied by alleviation of the behavioural phenotype of the mice [122]. This evidence concerns the gene APP and Alzheimer disease.