For example, SOCS1 expression level could be elevated by IL‐6/STAT3 signaling pathway, whereas high level of SOCS1 does not negatively feedback inhibit IL‐6/STAT3 signaling, but rather inhibits IFN‐γ/STAT1 signaling pathway and suppresses Th1 differentiation, that is, SOCS1 induces Th17 generation in IL‐6/STAT3‐mediated Th17 differentiation process.[33] Therefore, T cell specific knockout Socs1 could protect mice from EAE (a Th17‐dependent autoimmune disease model).[33b] Recently, using whole exome/genome sequencing, Hadjadj et al. The gene discussed is IFNG; the disease is autoimmune disease.