There have already been many findings in the search for biomarkers for response to treatment in rheumatoid arthritis. However, it lacks validation of the majority. In many cases because the necessary experiments have not been carried out. In addition, there are other possible sources of biomarkers that have not been sufficiently explored such as DNA methylation, gene expression in cell subpopulations, or cell function tests. We intend to fill some of these gaps by taking advantage of the samples obtained in previous studies and the new ones that will be obtained in this project. The studies we intend to perform include replication of the main results with genetic biomarkers for response to rituximab and tocilizumab. Contribution to similar studies of response to abatacept. Complete already initiated DNA methylation analyses of cellular subpopulations in response to MTX and TNF inhibitors, as well as gene expression studies, carbamilated anti-protein autoantibodies, and serum proteomic studies. Start new searches in promising areas: collection of urine samples to replicate results of a metabolomic study in response to TNFi; and ex vivo experiments of induction of monocyte apoptosis and phenotype in flow cytometry reflecting the suppressive activity of the Treg. Our goal is that these analyses contribute to establishing a panel of biomarkers that jointly used to guide the treatment of patients with RA.