The pharmacologic advantage of the dual ETAR/ETBR-antagonist is to target not only OC cells expressing ETAR, hampering the ZEB1/YAP interplay, but also to interfere with tumor microenvironment (TME) elements, such as cancer-associated fibroblasts, blood, lymphatic, and immune cells, which mainly expressed ETBR [9, 15, 44], representing a feasible approach which may target ET-1R-driven regulatory circuits in the HG-SOC ecosystem. This evidence concerns the gene EDNRA and cancer.