In murine cortical neurons, silencing the FTD-associated gene granulin (GRN) decreases the expression of extra synaptic NR2B-containing NMDAR (Longhena et al., 2017); on the other hand, hyper-phosphorylated tau enhances glutamate release and produces an overactivation of the same receptor ending with neuron death, that can eventually be reduced by stimulating its reuptake through the astrocytic glutamate transporter 1 (GLT1)/excitatory amino acid transporter 2 (EAAT2) (Decker et al., 2016). The gene discussed is GRN; the disease is frontotemporal dementia.