In transgenic mice engineered to overexpress ACKR1 in endothelial cells (via a preproendothelin promoter/enhancer), ACKR1 decreased the pro-angiogenic properties of ELR+ CXC chemokines (44), whereas ACKR1 deficient mice showed increased levels of these chemokines as well as increased angiogenesis in a model of prostate adenocarcinoma (35). The gene discussed is ACKR1; the disease is prostate adenocarcinoma.