Moreover, we have shown that the cellular sunitinib levels are not decreased in HT-29 sunitinib resistant cells in vitro. Since sunitinib inhibits the vascularity in both tumor models to the same extent, the resistance phenotype does not seem a consequence to hypoxia-induced growth factor production in the tumors or mobilization of growth-factor producing myeloid cell populations [31] with consequent switch of the endothelial cell compartment from dependence on VEGFR signaling to other signaling pathways (i.e. EGF/EGFR or HGF/c-MET supported signaling) [16]. The gene discussed is MET; the disease is neoplasm.