In line with this, enrichment of TNF-induced gene transcripts in synovial samples of early RA patients was associated with poor response to tocilizumab [141], and in the previously mentioned study by Dennis et al. [70] a serological cytokine signature (sICAM1high/CXCL13low) that correlated with myeloid TNF-rich mechanisms at the synovial level was negatively associated with the ACR50 response to tocilizumab (20%), whereas the opposite profile, surrogate of a lymphoid synovial signature (sICAM1low/CXCL13high), strongly predicted clinical response to IL-6R blockade (ACR50 69%). This evidence concerns the gene IL6R and rheumatoid arthritis.