According to the well-known role of ET-1 as a mitogenic factor for cancer and stromal cells (Rosanò et al., 2013; Caprara et al., 2014; Tocci et al., 2019), the addition of exogenous ET-1 increases cell proliferation between 24 and 72 h, while the addition of both the ETAR and ETBR antagonists, BQ123 and BQ788, respectively, completely blocked ET-1 effects, supporting the presence of an ET-1 autocrine loop involving both receptors (Figure 2A). The gene discussed is EDNRA; the disease is cancer.