Studies have demonstrated that continuous activation of JAK/signal transduction and activation of transcription (STAT) signaling in RA synovial joints could induce a high level of matrix metalloproteinase gene expression, apoptosis of chondrocytes, and most prominently, apoptosis resistance of inflammatory cells in the synovial tissue, supporting that therapeutics targeting the JAK pathway may provide symptomatic relief for RA [9]. The gene discussed is SOAT1; the disease is rheumatoid arthritis.