Moreover, using a combination of in vitro studies with recombinant proteins, Abi1(−/−) and Crk(−/−) MEFs, and genetically modified GBM cells, our studies show that Abi1 functionally suppresses Crk binding to Abl, functionally suppresses Crk Tyr251 phosphorylation, and functionally suppresses Crk-mediated enhancement in cell motility and invasion. This evidence concerns the gene CRK and glioblastoma.