IL6 and neoplasm: IRF9 is essential for the transcription of interferon-stimulated genes involved in the Type I and III interferon (IFN) signaling pathways, which are critical for innate immune responses to viral infections and other stress signals; then, its dysregulation can lead to excessive inflammation with the production of pro-inflammatory cytokines (e.g., IL-6 and TNF-α), which overrides the benefits of the IFN-III response on intestinal epithelial cells, contributing to chronic inflammatory diseases and creating a tumor-promoting environment [57].