In human samples the level of SOCS2 expression was negatively correlated with NASH: SOCS2 overexpression in macrophages suppressed inflammation and apoptosis via inhibiting NF-κB signaling pathway, whilst SOCS2 knock-down in macrophages caused an increased activation of NF-κB. The gene discussed is SOCS2; the disease is metabolic dysfunction-associated steatohepatitis.