The transition from dormant to the angiogenic state of the tumor is termed the “angiogenic switch” and is caused by a shift in the balance of anti- and pro-angiogenic factors.6 It is regulated by environmental factors and by genetic alterations that act to either up-regulate pro-angiogenic factors, such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) and/or down-regulate inhibitors of angiogenesis, such as angiostatin, endostatin, thrombospondin and interferons.7 The gene discussed is FGF2; the disease is neoplasm.