Since our current and previous studies [36] have shown that co-modified fibrinogen increases macrophage secretion of IL-1β, TNF-α, and TGF-β, chronic indirect stimulation with Mφ-SNFIB-MAA-CIT could lead to a robust pro-fibrotic phenotype in endothelial cells, further contributing to perivascular fibrosis in RA. The gene discussed is TGFB1; the disease is rheumatoid arthritis.