The fall in circulating hVEGF in the Bev-R group occurred in the context of a concurrent increase in VEGF staining in those tumors, which may reflect an on-target effect of the treatment whereby the tumor is compensating for bevacizumab therapy by increasing VEGF, but could also be explained by the broader hypoxia response that would stimulate further expression of VEGF. This evidence concerns the gene VEGFA and neoplasm.