Since the activation of this protein kinase is associated not only with neuroinflammation but also with many other pathophysiological features of AD, a novel therapeutic approach based on the selective inhibition of p38α MAPK could potentially modify multiple mechanisms leading to neurodegeneration and thus be more effective in alleviating the symptoms of cognitive decline and memory loss in patients suffering from AD. The gene discussed is WEE1; the disease is Alzheimer disease.