In different autoimmune diseases, such as psoriasis or systemic lupus erythematosus (SLE), it has been shown that inert self-DNA fragments that are released, for example, by dying cells, can be bound by the antimicrobial peptide LL37/Cramp to form complexes that can trigger recognition of self-DNA by TLR7/TLR9 by pDCs and the secretion of type I IFNs [48, 51–53]. This evidence concerns the gene TLR9 and systemic lupus erythematosus.