For example, during SLE and rheumatoid arthritis, isolated human monocytes display increased production of IL-1β, IL-6, and TNF-α [109,110], activated PI3K/mTOR and MAPK signaling pathways [111], high expression of CD80, CD86, and HLA-DR [112], suggesting a better capacity of presenting antigens to T cells, including the presentation of self-antigens to autoreactive T cells. This evidence concerns the gene IL1B and rheumatoid arthritis.