Although the pristane-induced lupus model shows a type I IFN signature and requires IFN I for autoantibody production and disease development, IFNγ is overproduced and plays a crucial role in various other mouse models such as MLR-Faslpr/lpr, Sle1b, and Wiskott-Aldrich syndrome (WAS) chimera mice31,38–40. This evidence concerns the gene IFNG and systemic lupus erythematosus.