This spectrum of effects arises from GBPs’ tissue-specific expression, interactions with the TME—immune cells (e.g., tumor-associated macrophages, T lymphocytes), stromal fibroblasts, cytokines (e.g., interferon-gamma, TNF-α), and co-activated pathways (e.g., EGFR, Wnt, Stat3)—and their interferon-driven regulation [3,54]. This evidence concerns the gene IFNG and neoplasm.