For example, the vascular endothelial growth factor (VEGF)-A and VEGF receptor 2 (VEGFR2) have been found upregulated in PWS [50], which may lead to the activation of VEGFR2 and subsequently activate MAPK; (2) environmental stresses, such as hypertrophied and disorganized collagenous fibers in matrix compositions and changes in blood flow shear forces in dilated PWS vasculatures; (3) alterations in EphB1 and EfnB2 signaling pathways. This evidence concerns the gene EPHB1 and Prader-Willi syndrome.