Rheumatoid arthritis (RA ) is a chronic inflammatory joint disease that is heterogeneous in nature. The heterogeneity is reflected by the variation in responsiveness to virtually any treatment modality. Since our understanding of the molecular complexity is incomplete and criteria for categorisation are limited, we mainly consider the disease RA as group average. A powerful way to gain insight into the complexity of RA has arisen from DNA microarray technology, which allows an open-ended survey to comprehensively identify the genes and biological pathways that are associated with clinically defined conditions. During the last decade encouraging results have been generated towards the molecular description of complex diseases in general. Here, I describe developments in genomics research that provide a framework to increase our
understanding of the pathogenesis and the identification of biomarkers for early diagnosis, prognosis and stratification, aimed at a personal medicine approach in RA .