The stimulation of tumor necrosis factor-α (TNF-α) and IL-1β could induce the expression of miR-146a/b and miR-155 in RA synovial fibroblasts remarkably, providing the evidence that miRNAs not only contribute to various aspects of RA pathogenesis, but may also be changed by the inflammatory milieu of resident cells in RA joints [18,19]. The gene discussed is IL1B; the disease is rheumatoid arthritis.