Increased Ras expression and activation of GSK-3 correlated with Aβ levels in the brain samples, implying that Aβ might elicit its toxic effects by modulating Ras-MAPK signaling and GSK3 activation, subsequently enhancing APP and tau phosphorylation and neuritic plaque and neurofibrillary tangle pathology development in AD. The gene discussed is APP; the disease is Alzheimer disease.