This is supported by reports that activating IP receptor by selexipag, treprostinil and iloprost [18, 83–89], β2-adrenoreceptors by oladaterol [90], or melatonin receptors by melatonin [91] is antifibrotic in vitro and in animal fibrosis models, and at the same time inhibits YAP/TAZ [18, 23, 91]. This evidence concerns the gene WWTR1 and fibrosis.