Altered vitamin C status in cancer patients can be attributed to changes in metabolism and signaling pathways related to oxidative and inflammatory processes inherent in the disease, as suggested by increased levels of lipid peroxidation products (e.g., MDA) and pro-inflammatory mediators (e.g., TNF-α, TGF-β, NF-κB, IL-10, and cyclooxygenase 2) [178,179]. This evidence concerns the gene NFKB1 and cancer.