Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by inflammation and joint damage that causes significant morbidity and mortality. Rapid and appropriate intervention by intensive treatments is prerequisite to halt joint damage and long-term functional disabilities. Recent progress in the treatment strategy has brought about paradigm shift for the management of RA, namely, the combined use of methotrexate, a synthetic disease-modifying anti-rheumatic drug (DMARD), and biologic DMARDs targeting TNF, IL-6 and T cells has revolutionized treatment of RA. Clinical remission is now realistic targets for the treatment, achieved by a large proportion of RA patients, which leads to structural remission without damage in bone and cartilage as well as functional remission. Furthermore, orally available small but strong molecules targeting signaling kinase are emerging. Oral administration of tofacitinib targeting the Janus kinase (JAK) is significantly effective than placebo in active patients with methotrexate-naïve, inadequately responsive to methotrexate or TNF-inhibitors. The efficacy was rapid and as strong as TNF-inhibitors. Multiple kinase inhibitors are currently developed. On the other hand, how differentially use multiple inhibitors remain unclear. Psoriatic arthritis (PsA) is a chronic and progressive inflammatory arthritis. Because PsA is a clinically heterogeneous disorder, we have tried to classify PsA by phenotypic differences of peripheral lymphocyte using 8-color flow cytometry and found that PsA can be divided to four types, activated Th17-dominant, Th1-dominant, both of them and neither of them. We currently try to treat patients with different bDMARDs based on the difference of lymphocyte phenotype, which may lead to precision medicine of PsA. Thus, differential use of biologics based on lymphocyte phenotype leads to a precision medicine for the treatment of inflammatory autoimmune diseases such as PsA and RA.