(1) Crosstalk between macrophages and epithelial/tubular cells includes several mechanisms: Human serum albumin (HSA)-induced EVs miR-199a-5p from TECs is reported to induce kidney fibrosis and inflammation by polarizing M1-type macrophages and accelerating DN progression by targeting the Klotho/TLR4 signaling pathway [152], or by stabilizing HIF-1α to promote glycolysis in M1 macrophages [153]. The gene discussed is KL; the disease is liver dysplastic nodule.