TGFB1 and neoplasm: CIT-013 may be further developed for treatment of gout.3 Activated neutrophils that engulf dying neutrophils by phagocytosis in the late stages of gout attacks can promote the production of TGFβ1 and eliminate the inflammatory response.4 Furthermore, non-inflammatory phagocytosis of dying neutrophils by macrophages is associated with spontaneous remission of gout flares.5 Meanwhile, although studies of TGFβ1 in the treatment of autoimmune diseases have failed due to tumour development, single or a few doses may be beneficial for acute gout therapy.