In our studies Sho down-regulation was not present in three other forms of protein misfolding disorders, these being the cytoplasmic accumulation of Tau in Tg(P301L)23027 mice [32], and parenchymal and vascular accumulation of Aβ and Bri peptide in TgCRND8 and TgADanPP7 mice, respectively [26], [33], [51]. This evidence concerns the gene ITM2B and proteostasis deficiencies.