A recent study found that anti-Ro60–positive SLE immune complexes containing Alu RNAs and Alu transcripts were up-regulated in whole blood samples from patients with SLE relative to control samples and established that aberrant expression of endogenous Alu RNAs stimulated a TLR7-dependent response that enhances the secretion of IFN-α, IL-6, and TNF-α41. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.