Given the abundance of endogenous TLR agonists in the TME, it will be of great interest to determine whether hepcidin released by macrophages and neutrophils in the TME, in response to endogenous TLR agonists, inhibits ferroportin on cancer cells as a paracrine factor and increases intracellular iron content and thereby cancer cell proliferation. The gene discussed is SLC40A1; the disease is cancer.