Although these TNF-α inhibitor drugs have significantly improved RA treatment, approximately 40% to 44% of patients do not respond to them adequately [18] and might present with complications such as the development of serious adverse effects, including severe infections, malignancies, congestive heart failure, demyelinating disorders, skin reactions, and drug-induced lupus [19] or a reduced efficacy of the therapy due to the immunogenicity of the drug [20]. The gene discussed is TNF; the disease is rheumatoid arthritis.