Further ex vivo research indicated that the activation and proliferative potential of early RA CD4+ T cells stimulated by the overproduction of proinflammatory cytokines such as IFN-γ and IL-17 and the reduced proportion of FOXP3+ Treg cells are reversed by exposure to PIM1 kinase inhibitors, thus effectively alleviating arthritis progression and cartilage destruction (98). The gene discussed is CD4; the disease is rheumatoid arthritis.