Previous studies support a protective role for both LXRs and PPAR-γ in SLE: LXR-α/β and PPAR-γ KO mice accumulate ACs in spleens, produce anti-nuclear autoantibodies and develop lupus-like syndrome with glomerulonephritis [20,29]. This evidence concerns the gene NR1H3 and drug-induced lupus erythematosus.