With the onset of RA, pro-inflammatory factors such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 are first released by intra-articular immune cells and macrophage-like synovial cells to promote the infiltration of various immune cells such as adaptive immune cells, T cells and B cells into the synovium, exacerbating the secretion of pro-inflammatory factors and worsening RA by a vicious feedback cycle [10]. Here, IL1B is linked to rheumatoid arthritis.