Replenishing the intracellularstores of SOCS3 with cell penetrating forms of SOCS3 has been shown to effectivelysuppress the devastating effects of acute inflammation in ConA, LPS or SEB-inducedhepatitis models [45].Attenuated liver injury in STAT1–/– andIFN-γ–/– mice in response to ConA was associated withenhanced SOCS3 activation Whereas, decreased SOCS3 activation inIL-6–/– mice seem to result in enhanced hepatitis inresponse to ConA [46]. The gene discussed is STAT1; the disease is Hepatitis.