Induction of NETs by the effect of IFN-α and “two-receptor” ligation of RNP-IC may be part of an amplifying process of disease propagation that enhances the exposure of autoantigens (i.e., DNA) and endogenous adjuvants (e.g., LL37) and stimulates further IFN-α production in SLE. The gene discussed is IFNA1; the disease is systemic lupus erythematosus.