In order to further gain insight into the in vivo function of YAP signaling, and to further extend studies to potential pharmacological treatment approaches for IPF, we next sought to determine whether pharmacological intervention with a known suppressor of the YAP-TEAD transcriptional complex and FDA approved compound, verteporfin (VP), could reduce fibrotic burden in vivo29,30. The gene discussed is YAP1; the disease is idiopathic pulmonary fibrosis.