These network relationships are not only dictated by treatment but also by environmental factors, such as endocrine-active substances (EASs) and endocrine-disrupting chemicals (EDCs) that, by altering the activity of the immune system, can contribute to setting an unhealthy pro-tumor inflammation (PTI) (directly correlated to TNF-α and monocytes/macrophages action) [38,152,153,154], thus facilitating the oncogenic process via the promotion of tumor growth, survival, and metastasis and suppressing the anti-tumoral immune response, shaping pivotal TME characteristics [39]. This evidence concerns the gene TNF and neoplasm.