Moreover, Pawar RD et al. [46] reported that in nephritic MRL lpr/lpr mice, transient exposure to bacterial cell wall components LPS increased splenomegaly, production of DNA autoantibodies, serum IL-6, IL-12 as well as tumor necrosis factor (TNF) levels, and aggravated lupus nephritis (LN), which was a major complication of SLE and associated with high rates of morbidity [43]. The gene discussed is IL6; the disease is lobular neoplasia.