When Panx1, the putative effector of this downstream NMDAR-Src kinase-Panx1 pathway, is blocked, NMDAR fails to generate its characteristic nociceptive signaling, despite the fact that at the time of the experiments (10 days after neuropathy induction), NMDARs were already activated due to the neuropathic state, and also phosphorylated and with overexpressed NR2B subunits [1]. This evidence concerns the gene GRIN2B and neuropathy.