By contrast, activation of the IRE1 UPR branch appears to benefit AD pathogenesis, as shown in an AD model of Drosophila melanogaster, in which Xbp1 over-expression prevented Aβ toxicity (Casas-Tinto et al., 2011), as in a similar study in C. elegans, indicating that XBP1 is involved in defense against Aβ toxicity, presumably by increased autophagy (Safra et al., 2013). This evidence concerns the gene ERN1 and Alzheimer disease.