Interestingly, C5a stimulation of human endothelial cells led to increased expression of VEGF165 isoform and C5aR1 blockade by PMX53 attenuated tube formation mediated by VEGF, suggesting that the interplay between C5aR1 and VEGF plays a role in complement-dependent regulation of tumor angiogenesis [30]. The gene discussed is C5; the disease is neoplasm.