Recent studies have shed light on the role of inflammation as a significant carcinogenic mechanism, with alterations in the proinflammatory tumor microenvironment (TME), including heightened levels of interleukin 1β (IL-1β), interleukin 6 (IL-6), interleukin 8 (IL-8), interleukin 10 (IL-10), tumor necrosis factor-α (TNF-α), interferon gamma (INF-γ), reactive oxygen species (ROS), nitric oxide (NO), and reactive nitrogen species (RNS), known to promote cancer initiation, progression, and metastasis [4,5]. This evidence concerns the gene IFNG and neoplasm.