Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease primarily affecting the synovial joints, leading to progressive disability, premature death, and significant socioeconomic burden. Understanding the pathological mechanisms and developing effective therapies are crucial for improving patient outcomes. This review discusses the etiology, pathology, and modern pharmacologic treatments of RA, focusing on the four stages: triggering, maturation, targeting, and fulminant. The triggering stage involves the production of anti-citrullinated protein antibodies (ACPA), which is influenced by genetic and environmental factors. The maturation stage involves the development of immune responses to self-antigens, leading to ACPA production and immune system activation. The targeting stage involves the infiltration of immune cells into the joints, causing synovitis and joint damage. The fulminant stage is characterized by hyperplastic synovium, cartilage damage, bone erosion, and systemic consequences. Modern pharmacologic therapies for RA include conventional synthetic disease-modifying anti-rheumatic drugs (DMARDs), biological DMARDs, and novel small molecule DMARDs. Conventional DMARDs such as methotrexate, leflunomide, and sulfasalazine are effective in reducing disease activity and preventing joint deformity. Biological DMARDs, including TNF-α inhibitors, anti-CD20 antibodies, IL-6 inhibitors, and B-cell depletion agents, target specific pathways involved in RA pathology. These therapies have significantly improved disease remission and reduced joint damage. However, a significant proportion of RA patients do not respond adequately to current treatments, necessitating the development of new therapeutic options. The review highlights the importance of understanding the pathogenesis of RA and the potential of new pharmacological interventions to optimize treatment strategies.Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease primarily affecting the synovial joints, leading to progressive disability, premature death, and significant socioeconomic burden. Understanding the pathological mechanisms and developing effective therapies are crucial for improving patient outcomes. This review discusses the etiology, pathology, and modern pharmacologic treatments of RA, focusing on the four stages: triggering, maturation, targeting, and fulminant. The triggering stage involves the production of anti-citrullinated protein antibodies (ACPA), which is influenced by genetic and environmental factors. The maturation stage involves the development of immune responses to self-antigens, leading to ACPA production and immune system activation. The targeting stage involves the infiltration of immune cells into the joints, causing synovitis and joint damage. The fulminant stage is characterized by hyperplastic synovium, cartilage damage, bone erosion, and systemic consequences. Modern pharmacologic therapies for RA include conventional synthetic disease-modifying anti-rheumatic drugs (DMARDs), biological DMARDs, and novel small molecule DMARDs. Conventional DMARDs such as methotrexate, leflunomide, and sulfasalazine are effective in reducing disease activity and preventing joint deformity. Biological DMARDs, including TNF-α inhibitors, anti-CD20 antibodies, IL-6 inhibitors, and B-cell depletion agents, target specific pathways involved in RA pathology. These therapies have significantly improved disease remission and reduced joint damage. However, a significant proportion of RA patients do not respond adequately to current treatments, necessitating the development of new therapeutic options. The review highlights the importance of understanding the pathogenesis of RA and the potential of new pharmacological interventions to optimize treatment strategies.