The evidences from previous studies suggest that UA exerts its anti-cancer effects through the suppression of oncogenic growth signaling, such as that via phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) and epidermal growth factor receptor (EGFR)/mitogen-activated protein kinase (MAPK) pathways, and oncogenic transcription factors, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB), signal transducer and activator of transcription 3 (STAT3), and hypoxia-inducible factor-1α (HIF-1α), in several types of cancer [5]. This evidence concerns the gene NFKB1 and cancer.