TNFi drugs remain the most prescribed first-line biologics for patients with rheumatoid arthritis (RA). However, up to 40% of RA patients fail to respond to TNFi treatment. One explanation of non-response is the development of anti-drug antibodies and low drug levels.||Studies have consistently shown that:||Serum drug levels of monoclonal antibodies (such as adalimumab, certolizumab, infliximab) and the presence of anti-drug antibodies in samples taken at 3 and 6 months correlate with subsequent response at 12 months.|Non-responders and those who develop anti-drug antibodies are less likely to receive concomitant methotrexate or, if they do receive it, are on lower doses than responder groups.||However, it has not been proven that knowing that a patient had low drug levels or anti-drug antibodies would have improved the outcome; neither has it been shown that introducing or increasing the dose of methotrexate would reduce the formation of anti-drug antibodies, thereby improving outcome.||Observational data has revealed that RA non-responders, who exhibit adequate serum drug levels and no detectable anti-drug antibodies, have lower probability of response to another agent with the same mechanism of action (MOA), and may benefit in switching to a drug with a different MOA (12). RA non-responders, who have low detectable serum trough levels and detectable anti-drug antibodies, may benefit in switching to a less immunogenic drug (13, 14). These patients may have a predisposition of developing immunogenicity against the introduced foreign protein (12). Neutralising anti-drug antibodies against the TNFi etanercept or the T-cell co-stimulation inhibitor abatacept have not been detected (10, 12, 15). Furthermore whilst the use and dose of methotrexate at initiation of TNFi, has been associated with lower levels of anti-drug antibodies in our work and others (10, 16), it is not known if increasing the MTX dose once immunogenicity has developed reduces anti-drug antibodies and leads to improved treatment response.||Whilst algorithms have been proposed based on these tests (4, 17, 18), they have not been confirmed in a randomised controlled trial setting to show that the intervention (testing) is effective. Based on our preliminary work in an observational dataset, this feasibility study will allow us to design a definitive study to answer the important issue of whether pharmacological testing can be utilised as robust biomarkers to optimise future patient outcomes.||The next essential step, therefore, is to prove that introducing these tests improves clinical outcome. It is very important to do so because some clinicians are already requesting that their immunology laboratories introduce such tests; yet the tests themselves are expensive and have not yet shown efficacy (19). Conducting a clinical feasibility trial is one of the essential first steps in development of a full clinical trial to undertake process evaluation and assess the proposed study design, required number of participants and ensure optimum project completion.||The proposed trial is a clinical feasibility trial with the aim to ensure a realistic assessment and capability to conduct the full clinical trial. Participants with RA, commencing adalimumab or certolizumab will be randomised to determine whether providing test results on adalimumab/certolizumab drug levels and anti-drug antibodies at 4 weeks, 3 and 6 months to clinicians caring for patients with RA (n=15 patients) starting on treatment with adalimumab/certolizumab, improves the course of disease activity, compared to standard care (n=15 patients). Clinicians will be provided with feedback and a treatment algorithm. The feasibility of the study will be assessed by a number of factors including evaluation of recruitment, attrition, data completeness and process evaluation. The results will be used to inform the number of participants required to fully evaluate the intervention.