The significantly increased IGS in SLE patients of all ancestries with multiple autoantibodies, and the almost complete lack of the IGS in the 273 SLE patients without anti-RNP, -dsDNA, -Sm, -SSA, or -SSB provides support for the hypothesis that the IGS arises from downstream pattern recognition receptor signaling induced by endosomal TLRs binding to single- and double-stranded RNA and DNA containing immune complexes, as previously suggested (64). The gene discussed is RNPC3; the disease is systemic lupus erythematosus.