Over the last decade, many epigenetic mechanisms that contribute in the pathogenesis of autoimmune disorders have been revealed. MicroRNAs (miRNAs) are small, non-coding, RNA molecules that bind to messenger RNAs and disrupt the transcription of target genes. Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease in which a plethora of epigenetic changes take place. Current research on RA epigenetics has focused mainly on miRNAs. Genetic variance of some miRNA genes, especially miR-499, might predispose an individual to RA development. Additionally, altered expression of many miRNAs has been discovered in several cells, tissues and body fluids in patients with RA. MiRNAs expression also differs depending on disease’s stage and activity. Serum miR-22 and miR-103a might predict RA development in susceptible individuals (pre-RA), while serum miR-16, miR-24, miR-125a and miR-223 levels are altered in early RA (disease duration <12 months) patients compared to established RA or healthy individuals. Moreover, serum miR-223 levels have been associated with RA activity and disease relapse. What is more, serum levels of several miRNAs, including miR-125b and miR-223, could be used to predict response to RA treatment. Finally, miRNA analogs or antagonists have been used as therapeutic regimens in experimental arthritis models and have demonstrated promising results. In conclusion, the research on the miRNA alterations in RA sheds light to several aspects of RA pathogenesis, introduces new biomarkers for RA diagnosis and treatment response prediction and offers the opportunity to discover new, targeted drugs for patients with RA.