Furthermore, the finding that the knockout of nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor that maintains the cellular defence against oxidative stress, in mice with antibody-induced arthritis was associated not only with an increase in cartilage destruction but also with a high number of spontaneous fractures underlines the importance of reactive oxygen species for bone damage in arthritis models [12]. The gene discussed is NFE2L2; the disease is arthritic joint disease.