A different short sequence motif in L1 of NaV1.7 channels was identified as the site of CRMP2 binding (CRMP2 regulatory sequence, CRS) and administering CRS via a cell-permeable peptide or via an AAV9 capsid–caused channel internalization, thereby reducing DRG neuron excitability and ameliorating pain in a mouse model of neuropathic pain (26). Here, SCN9A is linked to congenital rubella syndrome.