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In accordance with its tissue damage\u2010associated expression pattern and its pleiotropic proinflammatory signalling capabilities, the <jats:styled-content style=\"fixed-case\">TWEAK<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">Fn14<\/jats:styled-content> system has been implicated in a huge number of pathologies. The use of <jats:styled-content style=\"fixed-case\">TWEAK<\/jats:styled-content>\u2010 and <jats:styled-content style=\"fixed-case\">Fn14<\/jats:styled-content>\u2010knockout mice identified the <jats:styled-content style=\"fixed-case\">TWEAK<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">Fn14<\/jats:styled-content> system as a crucial player in muscle atrophy, cerebral ischaemia, kidney injury, atherosclerosis and infarction as well as in various autoimmune scenarios including experimental autoimmune encephalitis, rheumatoid arthritis and inflammatory bowel disease. Moreover, there is increasing preclinical evidence that <jats:styled-content style=\"fixed-case\">Fn14<\/jats:styled-content> targeting is a useful option in tumour therapy. Based on a discussion of the signalling capabilities of <jats:styled-content style=\"fixed-case\">TWEAK<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">Fn14<\/jats:styled-content>, this review is focused on two major issues. 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