STAT3 and Hepatic fibrosis: Of note, IL-22 has been reported to inactivate the NLRP3 inflammasome signaling in HSCs and also to promote senescence of HSCs through the activation of the signal transducer and activator of transcription 3 (STAT3) and the suppressor of cytokine signaling 3 (SOCS3) in vitro, thus having a potentially beneficial effect on hepatic fibrosis [84, 85].