These analyses revealed the important roles of PI3K-Akt signaling pathway and lipid metabolism process in the pathogenesis of RA, and the potential roles of cytokine–cytokine receptor interaction, leukocyte–cell adhesion, lymphocyte differentiation, and T cell activation in RA, suggesting that abnormal expression or dysfunction of TIMP4 may be an important factor in the pathogenesis of RA. The gene discussed is AKT1; the disease is rheumatoid arthritis.