Nav1.6, distributed in the central and peripheral nervous systems, has been previously reported to be related to infantile epileptic encephalopathy (46, 47, 48), and recent studies have reported that the gain-of-function mutation of Nav1.6 increased trigeminal ganglia neuron excitability in trigeminal neuralgia (49), whereas Nav1.6 knockdown ameliorated mechanical pain behavior in models of local inflammation and neuropathic pain (50, 51). This evidence concerns the gene SCN8A and genetic developmental and epileptic encephalopathy.