Abstract

In this viewpoint, we summarise three different lines of evidence suggesting that current biological therapies directed at different molecules or cells have similar efficacy in rheumatoid arthritis and target similar populations of patients; therefore, distinct biological effects of targeted therapies may not account for differences in response. Moreover, currently available individual biomarkers or multiple biomarker sets do not provide information beyond that conveyed by clinical disease activity. Smart and novel research designs will have to be developed to find pertinent biomarkers. Until then, the focus of clinicians may have to solely rest on clinical disease activity assessment and targeting remission or low disease activity rapidly.