Both effects on channel gating of the F1800I mutation in the S6 helix of the fourth repeat are very similar to the electrophysiological effects reported for a deletion variant of the corresponding phenylalanine in the S6 helix of the third repeat of CaV2.1 (ΔF1502) found in patients with congenital ataxia and hemiplegic migraine (32), thus, supporting the causative role of mutations of this highly conserved amino acid in the pore domain of CaV2.1. This evidence concerns the gene CACNA1A and familial or sporadic hemiplegic migraine.