In addition to its association with SLE pathogenesis (22) and disease activity and flare (92, 93), BLyS has been shown in previous studies to be elevated as patients transition from autoantibody positivity to clinical disease and transition to classified SLE (1, 2), with blockade of BLyS (23, 24), as well as type I IFN receptors (25, 26) and IFN-γ (27) that drive BLyS, having the potential to improve disease outcomes in subsets of SLE patients. Here, IFNG is linked to systemic lupus erythematosus.