Proteins involved in ECM degradation and remodeling (e.g., CAIX, integrins β3, αvβ3 and αvβ5, PLOD2, MMP-2, MMP-9); EMT (e.g., CBF1, ZEB1, TWIST1); chemokine receptors (e.g., CXCR4, CCR5); cytoskeleton dynamics (e.g., cyclin G2); hemostasis (e.g., TF, factor VII); the pro-motility receptor, EphA2; and the cation channel protein, TRPC6, have been shown to contribute to GBM migration and invasion in response to hypoxia. The gene discussed is PLOD2; the disease is glioblastoma.