of hepcidin. Although the labile iron pool increases with serum transferrin-bound iron in this simulation, this is only because the model does not include the action of hepcidin in reducing duodenal export of iron. Expression and secretion of hepcidin will have a global effect of reducing the labile iron pool.

Hereditary Haemochromatosis Simulation {#hereditary-haemochromatosis-simulation .unnumbered}
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Hereditary haemochromatosis is the most common hereditary disorder with a prevalence higher than 1 in 500 [@Asberg2001Screening]. Type 1 haemochromatosis is the most common and is caused by a mutation in the HFE gene leading to a misregulation of hepcidin and consequent systemic iron overload.

A virtual HFE knockdown was performed by reducing 100-fold the rate constant for HFE synthesis in the model, to create a simulation of type 1 hereditary haemochromatosis. The simulation was run to steady state and results were compared with experimental findings.

Qualitative validation showed the [*in silico*]{} HFE knockdown could reproduce multiple experimental findings as shown in Table \[table:tableHFEKO\]. Quantitatively the model was unable to reproduce accurately the finding that [*Hfe -/-*]{} mice have 3 times higher hepatic iron levels [@Fleming2001Mouse]. This was due to the fixed intercellular transferrin bound iron concentration in the model, unlike in [*Hfe -/-*]{} 