Mechanistically ct-EMAP II suppresses primary and metastatic tumor growth through inhibition of endothelial cell adhesion to fibronectin [11], disrupts alveolar epithelial type II to type I cell transdifferentiation [12], regulates pulmonary cell-cell cohesion, aggregation, and lung assembly [13], blockade of fibronectin matrix assembly via α5β1 integrin [9], [11], and interference with vascular endothelial growth factor (VEGF) induced pro-angiogenic signaling [14]. Here, FN1 is linked to metastatic neoplasm.