Further studies should attempt to clarify whether ET-1, through distinct β-arr1-complexes with YAP and mutp53 can recruit or interact with factors, such as HIF-1α, β-catenin, or NF-κB, to orchestrate interconnected pathway network regulating tumor growth and progression in HG-SOC, and in other types of cancer harbouring gain of function TP53 mutations. The gene discussed is YAP1; the disease is neoplasm.