Rheumatoid arthritis (RA) is a complex autoimmune disorder characterized by chronic inflammation of the joints, leading to joint damage, disability, and systemic complications. The etiology of RA involves a complex interplay between genetic susceptibility and environmental factors, with genomic variants playing a crucial role in disease pathogenesis. This paper presents a comprehensive review of current understanding regarding the genomic variants implicated in RA and their contribution to unraveling the genetic susceptibility and immunological mechanisms underlying the disease. Genome-wide association studies (GWAS) have identified numerous genomic loci associated with RA susceptibility, highlighting the polygenic nature of the disease. These loci often contain genes involved in immune regulation, such as those encoding cytokines, cell surface receptors, and signaling molecules. Furthermore, advances in sequencing technologies and bioinformatics have enabled the identification of rare and low-frequency variants with significant effects on RA risk, providing deeper insights into the genetic architecture of the disease. In parallel, research efforts have elucidated the immunological mechanisms driving RA pathogenesis, involving dysregulated immune responses, aberrant activation of immune cells, and production of autoantibodies targeting self-antigens. The integration of genomic data with immunological studies has revealed intricate networks of gene interactions and pathways implicated in RA development and progression.