The pathophysiology of ACD/AI involves immune activation in response to tumour antigens with release of several pro-inflammatory cytokines by immune cells, including interleukin (IL)-1, IL-6, IL-22, tumour necrosis factor (TNF)-α, interferon (IFN)-γ, and transforming growth factor (TGF)-β which stimulate hepatic synthesis of hepcidin. This evidence concerns the gene HAMP and neoplasm.