Grohmann and colleagues demonstrated that the oxidative hepatic environment in obesity restrained the STAT1 and STAT3 phosphatase TCPTP, which led to potentiate STAT1 and STAT3 signaling, and further increase the risk of developing NASH and HCC in the setting of nutritional excess (82). Here, PTPN2 is linked to metabolic dysfunction-associated steatohepatitis.