A connection between inflammation and carcinogenesis has long been known, but the precise mechanisms are just beginning to be understood. NF-κB proteins, transcription factors which integrate stress signals and orchestrate immune responses, have also recently been linked to carcinogenesis. Hallmarks of cancer development include self-sufficiency in growth signals, insensitivity to growth-inhibitors, evasion of apoptosis, limitless replicative potential, tissue invasion and metastasis, and sustained angiogenesis. NF-κB signaling has been implicated in each of these hallmarks, and recent experimental studies have illuminated the mechanistic pathways by which NF-κB signaling contributes to these aspects of carcinogenesis. This review will focus on recent experimental data supporting the hypothesis that inflammation promotes carcinogenesis, and that NF-κB signaling is at the heart of such inflammation.