Our work elucidated the reciprocal activation of VEGF and CDK7 in angiogenesis, because VEGF promoted CDK7 expression and CDK 7 inhibition suppressed angiogenic activity of endothelium and VEGF secretion of RCC cells, indicating CDK7 as a pivotal new regulator of angiogenesis in both endothelial cells and RCC cells, and suggesting that CDK7 pharmacologically is a novel target for antiangiogenic therapy and provides the basis for a new therapeutic application of the CDK7 inhibitor, THZ1, as an antiangiogenic agent. The gene discussed is CDK7; the disease is renal cell carcinoma.