Rheumatoid arthritis (RA) is a chronic autoimmune disease affecting multiple joints and causing adverse effects on organs. Early diagnosis, aggressive treatment, and disease-modifying anti-rheumatic drugs (DMARDs) have improved the management and long-term prognosis of the disease. The global prevalence of RA is increasing, primarily in women, and is associated with disability and mortality. The prognosis depends on the disease stage at diagnosis; early diagnosis can prevent or delay disease progression in 90% of patients, preventing irreversible joint damage and disability. However, non-coding RNA (ncRNA), including microRNA and long ncRNA (lncRNA), which are small, non-coding segments of RNA that regulate gene expression, has been discovered to be deregulated in diseases like RA, potentially contributing to its pathogenesis, progression, and treatment. Pre-clinical RA, characterized by auto-antibodies and biomarkers before clinical RA, is a stage of RA research aimed at the early diagnosis and control of immunological abnormalities. For instance, SNP rs2850711 in lnc00305 links RA susceptibility to the response of miR-10a to methotrexate (MTX) treatment, and ncRNA plays a crucial role in refractory RA by regulating drug sensitivity. Lower miR-20a expression in rheumatoid arthritis synovial fibroblasts (RASFs) activates Janus Kinase (JAK)-mediated inflammation, promoting cell proliferation and apoptosis resistance. This study highlights changes in ncRNAs, disease progression, and novel therapeutic targets and strategies.