mice where there is an increase in transferrin saturation as a result of increased intestinal iron absorption [@Fleming2001Mouse]. Despite fixed extracellular conditions the model predicted an intracellular hepatocyte iron overload which would be further compounded by the systemic effects of the misregulation of hepcidin. The simulation recreated increased ferroportin levels despite the expression of ferroportin remaining the same as wild type which was consistent with mRNA measurements from Ludwiczek [*[*et al.*]{}* ]{} [@Ludwiczek2005Regulatory]. mRNA based experiments can be used to validate expression rates and protein assays are able to validate steady state protein concentrations as both expression rates and steady state protein concentrations are available as results from the computational model. The model of haemochromatosis was also able to replicate the dynamics of experimental responses to changing dietary iron conditions. An approximate 2-fold increase in hepatic ferroportin expression is caused by increased dietary iron in both haemochromatosis and healthy mice [@Ludwiczek2005Regulatory]. The model presented here recreated this increase with increasing intercellular iron as can be seen in Figure \[fig:IronChangeFPN\].

HFE knockout has been shown to impair the induction of hepcidin by iron in mouse [@Ludwiczek2005Regulatory], and human [@Piperno2007Blunted] hepatocytes and this was seen in the computational model as increasing transferrin 