Apart from exacerbating the inflammatory cascade, macrophages recruited into the renal tissue with the participation of chemokines are believed to contribute to the increased production of fibrotic factors, e.g., TGF-β1 (transforming growth factor β1) and PDGF (platelet-derived growth factor), which elevate the production of extracellular matrix and type IV collagen and exacerbate renal fibrosis, which could explain the higher risk of renal function deterioration and graft loss in this group of kidney recipients [2]. The gene discussed is TGFB1; the disease is renal fibrosis.