It is, indeed, well accepted that inflammation had a great impact on the stimulation of tumor-growth, invasiveness and angiogenesis [43] and that the over-expression of IL-1beta by the tumor microenvironment favors the process of carcinogenesis and strengthens invasiveness of already existing malignant cells [44,45], thus clearly influencing the outcome of anticancer therapy. The gene discussed is IL1B; the disease is neoplasm.