The synovial immunologic and inflammatory response of RA is tightly controlled by a variety of cellular and humoral process.[1] The JAK-signal transducer and activator of transcription (STAT) signaling pathway plays a role in mediating the function of inflammatory cytokines and growth factors associated with synovial inflammation and bone destruction in RA.[1,17] Tight regulation of the JAK signaling pathway has emerged as a crucial therapeutic strategy in RA. Here, SOAT1 is linked to rheumatoid arthritis.