PTPN1 and Hepatic fibrosis: Jianzhi Wu et al. reported FA as an agent that is capable of preventing all histological changes of CCl4-induced liver fibrosis in mice by suppressing hepatic oxidative stress, inflammatory response, macrophage activation, and HSC activation through the phosphorylation of AMPK via direct binding and the consequent inhibition of PTP1B (protein tyrosine phosphatase 1B) [164].