Since abatacept is not a cell-specific depleting antibody, we studied cell populations that triggered inflammatory responses in RA, such as Th1 (CD4+IFN-γ+) and Th17 (CD4+IL-17+), or played a regulatory role in immune responses, like FoxP3+ T cells (CD4+CD127-CD25+FoxP3+ T cells) and MDSCs (CD14+HLADRint/−CD15+CD33+ cells), as well as DCs (CD3-HLADR+CD1α+ cells) that provided a crucial link between innate and adaptive immune responses (Figure 2a). This evidence concerns the gene IFNG and rheumatoid arthritis.