Upon onset of experimental arthritis and during human RA, there is also a relative decrease in the number of Trem2-expressing resident lining macrophages and an increase in infiltrating CCR2- and IL-1β-expressing monocyte-derived macrophages, which is reversed again upon clinical disease remission where the anti-inflammatory tissue resident macrophage populations dominate again and the synovial barrier reforms (1, 5). This evidence concerns the gene IL1B and arthritic joint disease.