In the IFN signaling pathway, STAT1 is a critical mediator gene.(9,40) In the above-mentioned IFN pathway for regulating bone resorption, STAT1 mediates the effects of IFNG on both inhibition of RANKL-induced osteoclast differentiation(9,35,41) and secretion of IL-1, IL-6, and TNF.(36–38) In addition, in dexamethasone-treated peripheral blood mononuclear cell (PBMC) cultures, the inhibited IFNG expression suppressed expression of the STAT1 gene.(42) Furthermore, in lupus nephritis patients, basal expression of STAT1 was significantly higher in monocytes. This evidence concerns the gene STAT1 and lupus nephritis.