This is partly supported by the evidence that i) IGF-II receptor is expressed in a subset of Aβ-containing neuritic plaques and tau-positive neurofibrillary tangles in the AD brain [17] and ii) the receptor levels are altered in affected regions of the AD brain in individuals with PSEN1 mutations or carrying APOE ε4 alleles [17], [18] and iii) the levels of the IGF-II receptor are increased along with lysosomal enzymes in mutant APP transgenic mice overproducing Aβ peptides [19]. The gene discussed is APP; the disease is Alzheimer disease.