Recent experimental data suggest that HGF/MET [18], TGFβ/TGFβR [19], and CXCL12/CXCR4 [20, 21] enhance the invasive phenotype of GBM after anti-VEGF/VEGFR therapy and VEGFR inhibitors may up-regulate CXCR4 in a TGFβR signaling-dependent manner [22]. Here, CXCR4 is linked to glioblastoma.