Identifying this potential comorbidity may allow efforts to dissect the genetic basis of the condition to be targeted toward specific sets of genes that may have a role in both migraine and epilepsy pathophysiology, such as the ion channels enhancing excitatory neurotransmitter release (i.e., Cav2.1) or dendrite neuronal excitability and firing (Nav1.1), and their molecular interactors. Here, SCN1A is linked to epilepsy.