Together with our previous observations that neuronal deficiency of p38α‐MAPK reduces Aβ and phosphorylated tau proteins in the brains of AD mice (Schnöder et al., 2016, 2020, 2021), our serial studies support that inhibition of p38α‐MAPK is a novel therapeutic option targeting multiple pathogenic processes in AD. This evidence concerns the gene MAPT and Alzheimer disease.