Together, these data suggest that Abi1 and Crk impart a reciprocal regulation on Abl kinase (Crk positively regulates while Abi1 negatively regulates), and that loss of the Abi1 gene in GBM functions in part by enhancing the Crk Tyr251 Abl axis to promote aggressive behavior in tumor cells. The gene discussed is ABI1; the disease is glioblastoma.