Xie et al., 2019 report that the SNX8 expression level is significantly lower in AD patients and APP/PS1 AD mouse brain. Overexpression of SNX8 suppresses the accumulation of fragments of amyloid precursor protein (Aβ). Additionally, patients lacking SNX8 were shown to have heart development defects, intellectual disability, learning and language delay, and severe behavioral problems related to the hyperactive-impulsive and inattentive area (Vanzo et al., 2014; Rendu et al., 2014; Mastromoro et al., 2020). This evidence concerns the gene SNX8 and Intellectual disability.