However, the contribution of other immune pathways led to the identification of endotypes corresponding to specific phenotypes that, so far, has been poorly defined, as demonstrated by the relatively high upregulation of the Th17 signal in Asian AD compared with European AD skin, which could explain the predominance of well-demarcated, psoriasiform lesions in Asian patients compared to European ones but cannot explain why the inhibition of IL-17A failed to demonstrate clinical, histopathological, and transcriptomic benefits (Figure 1) [106,119]. The gene discussed is IL17A; the disease is Alzheimer disease.