LL-37 has been shown to enhance TLR3 signalling in response to viral dsRNAs that are poor agonists by themselves (Lai et al, 2011) and it can also complex with self-DNA and self-RNA in autoimmune disorders, altering internalisation and endosomal processing to induce inflammatory responses to otherwise non-immunogenic nucleic acids via TLR7, TLR8 and TLR9 (Lande et al, 2007; Ganguly et al, 2009). Here, CAMP is linked to autoimmune disease.