STAT3 and fibrosis: The results of animal experiments have shown that p-JAK2/JAK2 and p-STAT3/STAT3 protein levels were significantly higher in the fibrosis model group compared with those in the control group, suggesting that JAK2/STAT3 signaling was activated in the liver tissues of rats during dimethylnitrosamine-induced hepatic fibrosis and was involved in the development of hepatic fibrosis (40) (Figure 2).