There are several potential mechanisms of VM formation, such as epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs) [22, 23], and various signaling pathways that promote VM formation, including vascular endothelial (VE)-cadherin, erythropoietin-producing hepatocellular receptor A2 (EphA2), phosphatidyl inositol 3-kinase (PI3K), matrix metalloproteinases (MMPs), vascular endothelial growth factor receptor (VEGFR1), cyclic adenosine monophosphate (cAMP), focal adhesion kinase (FAK), and hypoxia inducible factor (HIF)-1a [24, 25]. The gene discussed is EPHA2; the disease is cancer.