The onset of RA is proceeded by a preclinical RA stage, wherein genetic factors such as shared-epitope-positive HLA-DRB1 alleles, PTPN22 variant and environmental stressors promote post-translational protein modifications such as citrullination or carbamylation, and generate neo-epitopes of autologous proteins such as fibrinogen, fibronectin, collagen, and vimentin. Here, VIM is linked to rheumatoid arthritis.