Previous studies in cellular AD models suggest a clear cause-effect relationship between Aβ accumulation and PTEN recruitment to spines, and they confirm that blocking PTEN activity, either by inhibiting its catalytic activity or by preventing its interaction with PDZ proteins at synapses (e.g., PSD-95) can prevent the exaggerated synaptic depression and cognitive malfunctions typical of AD models. The gene discussed is PTEN; the disease is Alzheimer disease.