In ovarian cancer cells, activation of ETAR, by mimicking hypoxia, induces the nuclear β-arr1/HIF-1α interaction and the recruitment of p300 to hypoxia response elements of gene targets, resulting in enhanced histone acetylation, transcription and thus release of HIF-1α targets, such as ET-1 and VEGF, required for tumor cell invasion and pro-angiogenic effects in ECs [58]. This evidence concerns the gene HIF1A and ovarian cancer.