Interestingly, we also found an increased expression of HSPs (HSP90 and HSP70) in FAD fibroblasts (Figures 5, 7, 8) which are involved in maintaining protein homeostasis through the regulation of protein folding and turnover via the proteasomal or autophagic pathways, which hold relevance in AD due to the accumulation of Aβ peptide and tau protein (Dou et al., 2003; Lu et al., 2014; Ou et al., 2014; Campanella et al., 2018). This evidence concerns the gene HSP90AA1 and Alzheimer disease.