In a study of neurological disorders, p38γ was found to phosphorylate tau protein at T181, which together with extracellular amyloid-β (AB), orchestrates neuronal dysfunction in Alzheimer’s disease, whereas a site-specific tau phosphorylation disrupts the PSD-95/tau/Fyn interaction and inhibits Aβ toxicity [14]. Here, MAPT is linked to early-onset autosomal dominant Alzheimer disease.