This observation may be explained in part by the lower (∼10-fold half-maximal inhibition) oxygen levels required to effect binding of 2-nitroimidazoles to cellular macromolecules vs that required to induce VEGF production (Leith and Michelson, 1995); in this regard, both tumour models are sufficiently hypoxic to induce VEGF production. The gene discussed is VEGFA; the disease is neoplasm.