Several human AD cell models, namely hiNs originating from sporadic and familial AD patients [27], hiNs carrying fAD APP and PSEN1 mutations [34] and hiNs knocked-out for the AD risk gene SORL1 [25, 32], recapitulate these endosomal defects similarly to what we observed in the BIN1iso1 overexpressing hiNs. This evidence concerns the gene PSEN1 and Alzheimer disease.