TRIF-dependent TLR-4 signaling leads to the production of IFN-α and β. IFN-β was increased in the spleens of mice that had received liposomes with nonbilayer phospholipid arrangements compared with healthy mice, and increased levels of IFN-α and β are reported in patients with SLE [34]. The gene discussed is TLR4; the disease is systemic lupus erythematosus.