Activated macrophages then release inflammatory factors that modulate Th17 cell responses, facilitating the recruitment and activation of additional proinflammatory immune cells at the damaged sites, and may contribute to the progression of renal fibrosis by enhancing the activity of TGF‐β.[46, 47] Therefore, this mechanism may serve as a novel therapeutic target for emerging drugs to reduce the risk of renal fibrosis in patients with NAFLD. Here, TGFB1 is linked to metabolic dysfunction-associated steatotic liver disease.