Excessive activation of the innate immune system involving toll-like receptor 7 (TLR7) has been recognized as an important pathogenic mechanism in SLE [127] and miR-3148, with a predicted binding site at the 3′-untranslated region (3′-UTR) of TLR7 mRNA, modulates the allelic expression of this gene. Here, TLR7 is linked to systemic lupus erythematosus.