What is the current research progress on the role of the JAK/STAT/mTOR pathway in liver inflammation during liver failure, and is it considered a core pathway in this process?

I am studying the regulatory network of liver inflammation in the pathogenesis of liver failure, especially acute‑on‑chronic liver failure (ACLF). My current focus is on the phosphorylation activation of the JAK/STAT pathway and its downstream mTOR signaling in mediating hepatocyte death, macrophage polarization, and the inflammatory storm. I would like to know the latest research progress on this pathway—for example, whether it involves intercellular crosstalk—and whether the JAK/STAT/mTOR axis is regarded as a core or upstream regulatory hub compared with classical inflammatory pathways such as NF‑κB and NLRP3 in liver failure. If there are relevant clinical translational studies (e.g., the application prospects of JAK inhibitors), a brief discussion would also be appreciated.