In previous studies in SLE, serum and plasma levels of Gal-3BP correlated with disease activity and with activation of interferon-related genes.12 In a recent study, the release of DNA-segments and Gal-3BP containing microvesicles was triggered upon stimulation of peripheral blood mononuclear cells of SLE patients by IFN-alpha, as well as via TLR-7 and TLR-9 agonists,15 which reinforces the concept of Gal-3BP as an interferon inducible protein directly involved in pathogenic events in SLE. Here, TLR9 is linked to systemic lupus erythematosus.