Considering that serum TNF levels are undetectable in unchallenged Gpatch2−/− mice (Fig. 4C, see pre-LPS serum TNF), it is not surprising that Gpatch2 mutants did not display an increased propensity for TNF-related arthritis, inflammatory bowel disease or heart valve disease (Fig. 3A–E), pathologies that are observed in several of our Tnf 3’ UTR mutant mouse strains [6, 7]. The gene discussed is GPATCH2; the disease is arthritic joint disease.