In this multi-omics analysis involving 27 bDMARD-naïve RA patients, we found that, compared to responders, IFN-γ is accumulated during anti-TNF therapy in non-responders, which attracts additional T cells into the synovial tissue via CXC motif chemokine ligand 10, forming a vicious cycle of resistance to anti-TNF inhibitors [37]. This evidence concerns the gene IFNG and rheumatoid arthritis.