Defective apoptosis and clearance of apoptotic bodies, which are common in SLE patients, determine the release of nucleic acids with subsequent production of ICs; the same nuclear antigens act as ligand for endosomal TLRs (TLR3, TLR7, TLR8, and TLR9) expressed by B cells and antigen presenting cells further contributing to (auto)antibodies production [16]. The gene discussed is TLR3; the disease is systemic lupus erythematosus.