By transcriptionally profiling the tumor ECs (TECs) isolated from ovarian cancer specimens poorly infiltrated by T cells, the authors describe a mechanism that relies on the interaction between endothelin B receptor (ETBR), found to be highly expressed by TECs, and its ligand endothelin-1 (ET-1), overexpressed in ovarian cancer cells. The gene discussed is EDN1; the disease is ovarian carcinoma.