After recognizing a pathogen and recruiting the adaptor protein MyD88, TLR4 triggers nuclear factor kappaB (NF-κB) transcription, which activates several signaling pathways that regulate Mφ functions, including phagocytosis, and increases levels of proinflammatory cytokines [e.g., inducible nitric oxide synthase (iNOS), interleukin (IL)-1β, cyclooxygenase-2, IL-6, and tumor necrosis factor (TNF)-α] directly involved in kidney injury 30, 31. This evidence concerns the gene TNF and urogenital neoplasm.