Current literature suggests that hypoxia produces NO, calcitonin gene-related peptide(CGRP), adenosine, hypoxia-inducible factor 1 (HIF-1), vascular endothelial growth factor(VEGF), and other regulatory mediators, which results in meningeal vasodilation, increased blood flow, and angiogenesis, leading to the phenotypic presentation of migraine [15, 16]. Here, VEGFA is linked to migraine disorder.