Regardless of whether a cancer results from a heritable mutation, research has indicated that most cancers are caused by dysregulation of up to 500 gene products [1]. These gene products include growth factors (e.g., EGF, VEGF, and IGF-1), growth factor receptors (e.g., EGF receptor), protein kinases (e.g., Src), inflammatory cytokines (e.g., TNF, IL-1, IL-6), inflammatory enzymes (e.g., COX-2, 5-LOX, PLA-2), proapoptotic proteins (e.g., TNF, Fas, TRAIL), antiapoptotic proteins (e.g., Bcl-2, Bcl-xL, cFLIP, IAP-1, IAP-2, survivin), tumor suppressors (e.g., p53, Rb), and transcription factors (e.g., NF-κB, AP-1, STAT3, HIF-1, PPARγ). One of the most significant pathways is the pro-inflammatory pathway activated through the transcription factor NF-κB. This transcription factor is activated by various risk factors, including grilled meat, fried foods, saturated fatty acids, chemical and physical stress, and environmental pollutants [2]. Once activated, NF-κB regulates the expression of gene products that mediate survival (e.g., antiapoptotic proteins bcl-2, Bcl-xL, cFLIP, IAP-1, IAP-2, and survivin), proliferation (e.g., COX-2, c-myc, and cyclin D1), invasion (e.g., 5-LOX, MMP-9, ICAM-1, ELAM-1, and VCAM-1), and neo-angiogenesis (e.g., VEGF, IL-8, TNF, and IL-1) [3]. Most agents that downregulate these pathways are highly specific for their targets (e.g., inhibitors of COX-2, VEGF, and EGFR).