In summary, the results of these experiments all demonstrated that anti-IL-6R Ab treatment (and IL-6 KO status) had much less effect than anti-TNF-α Ab treatment (or TNFR1 KO status) on the development of TB infection in mice, suggesting that TNF-α is much more important than IL-6 in defence against TB infection, and that there may be less need to limit the clinical use of IL-6 blockers out of fear of reactivating TB. The gene discussed is IL6R; the disease is tuberculosis.