Rheumatoid arthritis, or RA, is a type of chronic inflammatory disorder that is defined by inflammation of the joints, pain, and joint degeneration. Thus, although genetic predispositions play a role in RA development, they are insufficient to explain differences in the disease’s initiation and activity. Epigenomics, referring to changes in the phenotype of a gene or group of genes brought by modification of the DNA molecule without altering its base sequence, offers important information on RA’s multifactorial etiology. The present article aimed at discussing the various epigenetic features in RA such as DNA methylation, histone modification, and non-coding RNA. These changes include, hypomethylation of the pro-inflammatory genes and hypermethylation of the anti-inflammatory genes and this promotes inflammation in the body specifically in RA. Other epigenetic abnormalities causing distortion of disease pathology include dysregulated histone modifications and non-coding RNAs. Knowledge of these epigenetic changes have brought about the intervention strategies in the form of epigenetic therapies. Azacitidine, vorinostat and miRNA based therapies are some of the classes of drugs which demonstrate efficacy in preclinical and clinical trials. That nevertheless there are some limitations that researchers are yet to embrace regarding specificity, delivery, and the true interactions between epigenetics. It is proposed that the further research should be concentrated on the development of precise or pharmacogenomic medicine approaches, the combination of genetic and epigenetic aspects of the drug treatment. In this context, the present review of the epigenetic targets and therapies clearly brings out the possibilities of im-proving RA management and the quality of life of patients through epigenetic interventions.