The full clinical disease in ORAS may therefore be a “compound” phenotype where hyper‐inflammatory, TNF‐secreting haematopoietic (myeloid) cells cause TNF‐induced inflammation and cell death of both non‐haematopoietic cells with LUBAC downregulation, e.g. dermal fibroblasts, and haematopoietic cells (Fig 7D), thereby giving rise the organ‐specific hallmark symptoms panniculitis, diarrhoea and arthritis. This evidence concerns the gene TNF and arthritic joint disease.