Furthermore, in experiments, the myelocytes of mice overexpressing the human truncated DR3 molecule produced a soluble protein (vhDR3) that inhibited apoptosis induction in vitro in a similar fashion to Fas (57, 58), and experimental collagen-induced arthritis was enhanced in vivo in transgenic mice expressing vhDR3. The gene discussed is FAS; the disease is arthritic joint disease.