As PrPC propagates the neurotoxic signaling effects of Aβ46–48, this could implicate a mechanism whereby the effects observed by RanBPM overexpression in AD are, at least partially, a result of increased ubiquitination and proteasomal degradation of muskelin, leading to a defect in PrPC lysosomal degradation. Here, MKLN1 is linked to Alzheimer disease.