In summary, our studies have identified a novel regulatory network by which Abi1 and Crk reciprocally interact with Abl kinase to drive the malignant phenotypes in EGFR-expressing human GBM cells (Figure 7A, 7B) and functionally that the Crk non-canonical pathway is unleashed by the loss of Abi1. Here, EGFR is linked to glioblastoma.