Inflammatory mediators mainly produced by immune cells that infiltrate the kidney, but also renal cells in the kidney cortex, e.g., IL-6, TNF-α, IL-1β, and related signaling pathways such as JNK and NF-kB, were reported to significantly contribute to the development and progression of DN in mouse or rat streptozotocin-induced diabetic models of nephropathy [100,101,102], as well as major cancer hallmarks such as sustained proliferation, angiogenesis, immune escape and metastasis, which could facilitate renal cancer development with CKD [103,104]. This evidence concerns the gene IL1B and renal carcinoma.