The same authors showed that deficits in synaptic plasticity (i.e. BDNF-LTP) and in the persistence of spatial memory were fully reversed using rapamycin in the Ts65Dn model (Andrade-Talavera et al., 2015), indicating that targeting mTOR hyperactivation may be a novel pharmacotherapeutical approach for DS. The gene discussed is MTOR; the disease is Dravet syndrome.