This pro-metastatic state results in increased tumor proliferation via the secretion of interleukins (IL-6, IL-1β), tumor necrosis factor-α (TNF-α), and fatty acids, which activate STAT3, NF-κB, and PPARγ signaling pathways both in co-culture and in in vivo models of BCBM Zou et al. (2019); Seike et al. (2010); Wasilewski et al. (2017). The gene discussed is TNF; the disease is neoplasm.