Possible explanations for this observation are (1) simple cephalic vasodilation is not sufficient to trigger migraine pain, (2) vascular bed in the trigeminal region is different from extra-trigeminal region with regard to the released amount of CGRP and/or the CGRP receptor density, and (3) different combination of receptors involved in CGRP-induced vascular response in the trigeminal region. The gene discussed is CALCA; the disease is migraine disorder.