The mechanistic basis for inflammation-driven prostate carcinogenesis involves multiple interconnected pathways, such as NF-κB signaling activation driving transcription of pro-survival and proliferative genes, inflammasome-mediated secretion of IL-1β and IL-18 amplifying innate immune responses, oxidative stress-induced DNA damage creating genomic instability, and immunosuppressive microenvironment development facilitating tumor escape from immune surveillance [13-16]. The gene discussed is NFKB1; the disease is neoplasm.