By assessing tau phosphorylation and testing a catalytically mutant form of Fak, we could disfavor a change in tau phosphorylation (classically considered as one of the culprits in AD pathogenesis) as the cause of the modulation of tau neurotoxicity by Fak in Drosophila. A tau-PTK2B interaction was confirmed in the brains of a tau mouse model and human patients, since we observed an abnormal somatic accumulation of PTK2B with the appearance of tau oligomers and neurofibrillary tangles [28]. Here, PTK2B is linked to Alzheimer disease.