The pattern of gene expression that differed between the patient groups could suggest that canonical T1IFN pathway signaling is increased in peripheral blood CL monocytes of RA patients who are likely to respond to TNFi, whereas Jak/STAT-independent IFNB-IFNAR1 signaling is increased in NC monocytes of those who are not likely to respond to TNFi (Figure 4). Here, SOAT1 is linked to rheumatoid arthritis.