Stimulation of PBMC from RA patients by APL1 increased the proportions of Treg [30], induced apoptosis of activated CD4+ T cells, presumably through a Treg-dependent mechanism [31], and increased Treg suppression against APL1 responding effector T cells, at the same time decreased IL-17 that is produced by activated T cells [32]. This evidence concerns the gene CD4 and rheumatoid arthritis.