Rheumatoid arthritis is a chronic inflammatory disorder in which disease-modifying antirheumatic drugs (DMARDs), glucocorticoids, and targeted biologic or synthetic agents, such as tumor necrosis factor-alpha (TNF-α) inhibitors, Janus kinase (JAK) inhibitors, and interleukin-6 (IL-6) receptor antagonists, have improved disease control but have also modified infection risk profiles [5,6]. This evidence concerns the gene TNF and rheumatoid arthritis.