More studies aimed to investigate VM's formation mechanisms and signalling pathways (Fig.1) 28, including some factors related to tumour cell migration, invasion and matrix remodelling, such as vascular endothelial-cadherin (VE-cadherin) 29,30, epithelial cell kinase (EphA2) 10,31,32, phosphoinositide 3-kinase (PI3K), matrix metalloproteinase (MMPs), laminin 5 (Ln-5) γ2 chain 33–36, hypoxiainducible factor1-α (HIF-α) 37 and focal adhesion kinase (FAK) 38,39. This evidence concerns the gene EPHA2 and neoplasm.