Rheumatoid arthritis (RA) is the most common chronic arthritis in the world. RA is characterized by inflammatory joint synovitis and a resultant joint destruction. Patients with RA often display positivity for rheumatoid factor (RF) and/or anti-citrullinated peptide antibody (ACPA). Methotrexate is an anchor oral drug to treat RA. Biological agents, targeting TNF or IL-6R, are efficient treatment to RA which prevent joint destruction in patients with RA. However, patients with RA are heterogeneous. Joint destruction develops rapidly in some patients but slowly in others. ACPA and/or RF are not positive for all patients with RA. Moreover, positivities of ACPA and RF do not always correlate with each other. About 30% of patients with RA do not respond to biological treatment. What kind of factors determines the heterogeneity of RA? Genetic and environmental effects are assumed to explain these variance. In this review, we focus on genetic components and review how much variance of susceptibility to RA or RA phenotype can be explained and determined by genetic components. Recent technological advancement has enabled us to perform genome-wide association studies to detect susceptibility loci to complex diseases with an unbiased approach. More than 100 susceptibility loci to RA have been detected so far, and functional analyses have been successfully performed for some. Autoantibody status in patients with RA is strongly associated with HLA alleles. Unfortunately, detecting markers associated with response to treatment in patients with RA have not been very successful to date.