Therefore, a hypothesis could be envisaged that anemia could be aggravated by a high level of TNF-α via stimulating the expression of hepcidin, which could be eliminated by antagonizing TNF-α or blocking the caspase-3/8- and NF-κB-dependent pathways, which are involved in the delivery of TNF-α signaling. Here, NFKB1 is linked to anemia.