Yang generated an AD mouse model with IL-17A overexpression and Yang et al. (2017) reported that IL-17A does not exacerbate neuroinflammation, and Yang also demonstrated that IL-17A overexpression decreases the level of soluble Aβ in the CSF and hippocampus as well as improves the metabolism of glucose (Yang et al., 2017). This evidence concerns the gene IL17A and Alzheimer disease.