Given the large repertoire of DAMPs shown to activate TLR2, including anti-phospholipid autoantibodies, acute serum amyloid, HSPs, HMGB1, as well as several extracellular matrix components (95), some of which are known to be increased in DS serum (99), this elevation in TLR2 could potentially contribute to the state of exacerbated cytokine production characteristic of DS, via MyD88-independent pathways (100). The gene discussed is MYD88; the disease is Dravet syndrome.