Specifically, these mediators include n-6 PUFA-derived eicosanoids, and adipokines such as leptin and inflammatory cytokines (TNFα, IL-1β and IL-6) with a concomitant reduction in the anti-inflammatory adipokine, adiponectin (discussed below), which are produced in both visceral AT depots and surprisingly also within mammary AT depots, and collectively contribute to the development of a more severe BC phenotype via stimulating BC growth, invasion and metastasis. The gene discussed is IL1B; the disease is breast cancer.