For example, defects in regulatory T cells (Tregs) and an imbalance in helper T cell subsets (Th1/Th17) can sustain chronic immune responses.[18] Moreover, profibrotic factors such as transforming growth factor-β (TGF-β) and connective tissue growth factor synergistically activate signaling pathways, further accelerating the fibrotic process.[19] These mechanisms suggest that SLE-associated RPF results from the interplay between immune system dysregulation and fibrotic responses. Here, CCN2 is linked to systemic lupus erythematosus.