The variable clinical expression of different mutations within the CACNA1A gene, the phenotypic heterogeneity amongst those affected by the same genetic mutation, the sometimes overlapping clinical phenotypes, and the high prevalence of migraine amongst all the mutations is interesting and suggests shared biological mechanisms between ion channel-mediated alterations in neurotransmission and cortical excitability in migraine and these other neurological conditions [80,81]. This evidence concerns the gene CACNA1A and migraine disorder.