The research has proven that CD74 could interact with APP to inhibit the production of Aβ, and CD74 changed the intracellular distribution of APP and disrupted normal trafficking of APP in neurons instead of reducing the secretion of sAPPα or sAPPβ, and thus, the APP-CD74 signaling pathway was crucial for AD pathology (Matsuda et al., 2009; Kiyota et al., 2015). This evidence concerns the gene APP and Alzheimer disease.