Our study has exemplified the complexity of cancer-TME interactions by demonstrating that continuous stimulation of TNBC cells by proinflammatory cytokines that are constantly expressed in breast tumors—such as TNFα + IL-1β—lead to a hybrid metabolic state that is characterized by elevated glycolysis as well as OXPHOS, and skew TNBC into a proinflammatory phenotype that is regulated by glycolysis in the cancer cells. The gene discussed is TNF; the disease is cancer.