In addition, as observed for EO771-derived tumors treated with the VEGFR tyrosine kinase inhibitor SU112248 [33], gremlinC141A overexpression efficiently inhibited tumor neovascularization, as demonstrated by the reduction of ve-cadherin mRNA levels and CD31+ area in gremlinC141A-EO771 tumors when compared to mock lesions (Figure 7C–7E). Here, CDH17 is linked to neoplasm.