Systemic　lupus　erythematosus　(SLE)　is　a　complex　autoimmune　disease　involving　injuries　in　multiple　organs　and　systems.　Exaggerated　inflammatory　responses　are　characterized　as　end-organ　damage　in　patients　with　SLE.　Although　the　explicit　pathogenesis　of　SLE　remains　unclear,　increasing　evidence　suggests　that　dysregulation　of　cytokine　signals　contributes　to　the　progression　of　SLE　through　the　Janus　kinase/signal　transducer　and　activator　of　transcription　(STAT)　signaling　pathway.　Activated　STAT　proteins　translocate　to　the　cell　nucleus　and　induce　transcription　of　target　genes,　which　regulate　downstream　cytokine　production　and　inflammatory　cell　infiltration.　The　suppressor　of　cytokine　signaling　1　(SOCS1)　is　considered　as　a　classical　inhibitor　of　cytokine　signaling.　Recent　studies　have　demonstrated　that　SOCS1　expression　is　decreased　in　patients　with　SLE　and　in　murine　lupus　models,　and　this　negatively　correlates　with　the　magnitude　of　inflammation.　Dysregulation　of　SOCS1　signals　participates　in　various　pathological　processes　of　SLE　such　as　hematologic　abnormalities　and　autoantibody　generation.　Lupus　nephritis　is　one　of　the　most　serious　complications　of　SLE,　and　it　correlates　with　suppressed　SOCS1　signals　in　renal　tissues.　Moreover,　SOCS1　insufficiency　affects　the　function　of　several　other　organs,　including　skin,　central　nervous　system,　liver,　and　lungs.　Therefore,　SOCS1　aberrancy　contributes　to　the　development　of　both　systemic　and　local　inflammation　in　SLE　patients.　In　this　review,　we　discuss　recent　studies　regarding　the　roles　of　SOCS1　in　the　pathogenesis　of　SLE　and　its　therapeutic　implications.