Cancer cells have developed various ways to activate HIF by inactivating tumor suppressor genes, e.g., PTEN and VHL, activating various oncogenes, e.g., c-MYC, and increasing the activation of various growth factor pathways, e.g., insulin-like growth factor 1 (IGF-1), IGF-2, and platelet-derived growth factors (PDGF) (Maxwell et al., 2001). Here, IGF1 is linked to neoplasm.