Mechanically, the pattern of gene expression that differed between the response and nonresponse groups suggested that canonical type I IFN pathway signaling via JAK/STAT was increased in peripheral blood classical monocytes of RA patients who were likely to respond to TNF inhibition, whereas JAK/STAT-independent non-canonical IFNβ-IFNAR1 signaling was increased in nonclassical monocytes of those who were not likely to respond to TNF inhibition (175, 226). Here, SOAT1 is linked to rheumatoid arthritis.