In the current study, CCl4 treatment activated NF-κB and increased p-NF-κB expression, whereas SLE treatment significantly decreased the expression level of p-NF-κB. Taken together, our findings demonstrate that SLE could attenuate the release of proinflammatory cytokines and inhibit the activation of NF-κB in the CCl4-induced liver injury. The gene discussed is NFKB1; the disease is injury.