Tuberculosis (TB) and other opportunistic infections (OIs) occur more frequently in patients with rheumatoid arthritis (RA), and this risk is elevated by the use of prednisone and certain biological disease-modifying antirheumatic drugs (DMARDs).1–3 This has been best documented for granuloma-inducing pathogens in the setting of tumour necrosis factor-alpha (TNF) blockade.4–9 For biological therapies with other mechanisms of action, and for small molecular therapies like tofacitinib, less is known. This evidence concerns the gene TNF and tuberculosis.