Future studies in FHM1 S218L mice, which express a more severe mutation that results in an even more enhanced gain-of-function of CaV2.1 channels and CSD susceptibility with additional neurological symptoms including seizures and cerebellar ataxia [39], may address whether the identified changes in gene expression in FHM1 R192Q are more pronounced when CaV2.1 channel activity is more affected. The gene discussed is CACNA1A; the disease is cerebellar ataxia.