While STEP61 levels are elevated in the cortices of several AD mouse models [22, 28], genetic ablation of STEP61 blocks Aβ-induced reduction in surface AMPAR and NMDAR expression [22, 25] and prevents memory loss and LTP impairment in AD mouse models [25, 26], suggesting a critical role of STEP61 in mediating Aβ-induced synaptic weakening and cognitive dysfunction in AD. The gene discussed is PTPN5; the disease is Alzheimer disease.