CIM6P/IGF2R has been implicated in several aspects of Alzheimer’s disease (AD): levels of CIM6P/IGF2R decrease with the presence of APOE4 alleles (Kar et al., 2006), and overexpression of CIM6P/IGF2R increases amyloid precursor protein processing and amyloid-beta (Aβ) production (Wang et al., 2015), a hallmark alteration in AD. Here, APP is linked to early-onset autosomal dominant Alzheimer disease.