Although a recent report suggests that BIN1 overexpression promotes the recovery of tauopathy-induced long-term memory deficits[32], loss of Bin1 in forebrain excitatory neurons didn’t alter memory performance in the contextual fear conditioning task, although this may reflect the strength of the training paradigm used here, or compensatory changes in circuitry[54]. The gene discussed is BIN1; the disease is tauopathy.