In contrast, and despite the fact that BPSM1m/mTNFR1−/− donors themselves never develop NLH (Supplementary figure 1d), WT recipients of BPSM1m/mTNFR1−/− bone marrow had NLH (Supplementary figure 2j), demonstrating that overexpression of TNF triggers NLH by acting on a nonhematopoietic component, and that the expression of TNFR1 in the hematopoietic compartment is not necessary for NLH, arthritis or heart valve disease. The gene discussed is TNF; the disease is arthritic joint disease.