This strategy harmonizes with the wealth of evidence that indicates that in a variety of cell lines, including cancer cells (e.g. SK-Hep1, PC-3; Park et al., 2011) and human umbilical vein endothelial cells (Namkoong et al., 2009; Zhang and Daaka, 2011), activation of PKA-CREB- or HIF-1α-dependent pathways increases both VEGF transcriptional activity and the formation of new blood vessels. The gene discussed is HIF1A; the disease is cancer.