The pathogenesis of PWS is yet to be established and potentially associated with somatic genetic mutations (GNAQ, PI3K), MAPK and PI3K aberrant activations, molecular phenotypes of PWS endothelial cells, overexpression of vascular endothelial growth factor (VEGF) and its receptor VEGFR, formation of an immature venule-like vascular system and gradual dilation causing vascular malformation (2). Here, VEGFA is linked to Prader-Willi syndrome.