TNF and renal fibrosis: In tissue injury, inflammatory cells (e.g., lymphocytes, monocytes/macrophages, dendritic cells, and mast cells) are recruited to injured sites.[117] These activated immunocytes produce profibrogenic cytokines and growth factors and trigger renal fibrosis.[55, 118] For example, proinflammatory monocytes/macrophages (M1) mediate tubular injury through the production of interleukin 6 (IL‐6), TNFα, IL‐12, and nitric oxide (NO) by iNOS.[118] TNFα reportedly promotes tubular apoptosis after kidney injury.