These clinical and/or preclinical models include (i) infusion or the systemic administration of migraine-inducing compounds such as nitroglycerin (NTG), CGRP, and pituitary adenylate cyclase-activating peptide-38 (PACAP-38) [10,11,12]; (ii) chemical (with inflammatory molecules or irritant substances) or electrical activation of the structures included in the TVS (e.g., meninges and trigeminal ganglia) [12,13,14]; and (iii) the induction of cortical spreading depression (CSD) over the cortex surface, which is considered as the neurophysiological correlate of migraine aura [15]. This evidence concerns the gene CALCA and migraine disorder.