ACTA1 and idiopathic pulmonary fibrosis: Selective inhibition of YAP/TAZ through the agonism of Gαs-coupled dopamine receptor D1 (DRD1), a G protein-coupled receptor (GPCR), in the IPF fibroblasts reversed the formation of profibrotic α-SMA-positive myofibroblasts and augmented matrix degradation in a TGFβ-rich profibrotic environment [7].