Since amplification of EGFR is an important driver of tumorigenesis in GBM (as evident from cancer genome sequencing analysis) [30, 39], we explored the Crk Tyr251/Abl axis in several GBM cells lines, that de-regulate EGFR, using phosphospecific antibodies to AblY245 and CrkY251 (Supplementary Figure S3). The gene discussed is CRK; the disease is glioblastoma.