These factors can either act directly on muscle cells to increase intracellular catabolic signaling pathways that induce muscle atrophy, as is the case for TNF-α [48] and TGF-β members [49] or, in the case of myeloid-derived nitric oxide and peroxynitrite, can contribute to skeletal muscle damage and degeneration [50], which are pathologic features and potential contributing factors of cancer cachexia [46]. The gene discussed is TNF; the disease is cancer.