To further dissect the role of iPs in AD-like pathology, we crossed APPPS1 mice to β5i/LMP7 deficient mice lacking exons 1–5 of the proteasome subunit beta type 8 (PSMB8) gene, which encodes for the catalytic iP subunit β5i/LMP7 and is inevitable for iP formation, resulting in a loss of iP assembly in LMP7 deficient mice [18]. This evidence concerns the gene PSMB8 and Alzheimer disease.