Two key activity-regulated paracrine factors, NLGN3 and BDNF, each promote neuron-to-glioma synaptic interactions in distinct ways: NLGN3 promotes the expression of genes encoding the AMPAR subunits GluA2 (GRIA2) and GluA4 (GRIA4) as well as TrkB2 (NTRK2), whereas BDNF–TrkB signalling promotes trafficking of translated AMPAR subunits to the postsynaptic membrane to modulate the strength (amplitude) of postsynaptic currents. This evidence concerns the gene NLGN3 and central nervous system cancer.