This adds to other mechanisms previously proposed: therapy-induced tumor hypoxia could activate HIF-1 and HGF/Met pathways that increase tumor invasiveness and TC intravasation (Paez-Ribes et al, 2009; Cooke et al, 2012); host responses that upregulate circulating pro-angiogenic factors (Ebos et al, 2007) could enhance vascular permeability and TC diapedesis; and the destabilization of inter-EC junctions and pericytes in host organs could promote TC arrest or extravasation (Chung et al, 2012; Welti et al, 2012). This evidence concerns the gene HGF and neoplasm.