As noted before, APP, which is involved in the AD pathogenesis, collaborates with its binding protein Fe65 via interaction between C-terminal Fe65-PTB2 and AICD.33 We engineered EXO via overexpression (OE) of Fe65 in HT22 cells by transfecting pCI-Fe65 plasmid. This evidence concerns the gene APBB1 and Alzheimer disease.