These anti-LL-37 and anti-HNP autoantibodies seem to have a dual role in SLE, first, by facilitating the FcγRII-mediated endocytosis of self-DNA-antimicrobial peptides by pDCs and further stimulating the TLR9-mediated type I IFN release, and second, by enhancing the NET release from IFN-primed neutrophils [43,49]. The gene discussed is IFNA1; the disease is systemic lupus erythematosus.