Seeking possible mechanisms underlying this effect, our group found that galectin-1 was induced in response to hypoxia through hypoxia inducible factor-1 (HIF-1)-independent, nuclear factor kappa B (NF-kB)-dependent pathway [55] and promoted angiogenesis in several tumor types [55,142], particularly those resistant to vascular endothelial growth factor (VEGF)-targeted therapies [33]. The gene discussed is LGALS1; the disease is neoplasm.