These clinical resemblances may correspond to common biological disturbances, as was recently demonstrated through the experimental generation of impaired N-glycosylation at the CaV2.1 (encoded by CACNA1A); impaired N-glycosylation led to a gain-of-function on the CaV2.1 channel (8), similar to those mutations causing FHM (17, 18). Here, CACNA1A is linked to familial hemiplegic migraine.