Beyond general immune dysregulation common to many autoimmune diseases, additional mechanisms have been proposed to explain the link between SLE and malignancy, including increased synthesis of the APRIL protein (which may promote apoptosis evasion and has been observed in diffuse large B-cell lymphomas in SLE), shared genetic predispositions involving tumour necrosis factor (TNF) and interferon pathways, possible overlap with secondary SS and the impact of immunosuppressive therapies [101]. Here, TNFSF13 is linked to synovial sarcoma.