YAP/TAZ triggers catabolism of glutamine and serine to maintain proline and glycine anabolism and promote collagen synthesis.[415] In the lung, AMPK inactivation in endothelial cells activates the expression of YAP, thereby inducing pulmonary fibrosis.[416] Researchers have revealed that dihydrotanshinone I (DHI), a lipophilic component from natural herbs, alleviates hepatic fibrosis via the inhibition of YAP/TEAD2.[417] Gli+ cell‐specific deletion of Yap/Taz in a UUO mouse model resulted in decreased ECM accumulation, myofibroblast recruitment, and interstitial fibrosis.[418]. The gene discussed is TEAD2; the disease is Hepatic fibrosis.