Finally, since several recent reports have observed by FISH the presence of large-scale genomic alterations in neural cells of AD patients related to AD pathogenesis (i.e. aneuploidy, X-chromosome instability, APP duplications...) [60–62], we decided to explore the potential existence of rearrangements in the DDIT3 gene, which would be responsible for the down-regulation of DDIT3 at mRNA and protein levels in AD (Figure 5). Here, DDIT3 is linked to Alzheimer disease.