Second, given that hepcidin is controlled by multiple competing stimuli (Huang et al., 2009), hepcidin might only influence the subsequent risk of infection when very strong down-regulatory signals from ID and erythropoietic drive overwhelm weaker up-regulatory signals from malaria and other infections (Casals-Pascual et al., 2012, Jonker et al., 2013). This evidence concerns the gene HAMP and malaria.