According to recent research, chemokine receptors (i.e., CCR1, CCR5, and CXCR3) are expressed by synovial NK cells, which can facilitate the recruitment of inflammatory cells (driven by their respective chemokines) into the RA synovium [16], prime effector myeloid cells, and aggravate arthritis by producing inflammatory mediators such as granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage (M)-CSF, and receptor activator of nuclear factor (NF)-kappaB ligand (RANKL) [17,18]. The gene discussed is CSF2; the disease is arthritic joint disease.