bound iron did not induce hepcidin as strongly in HFE knockdown.

Although an increase in transferrin receptor 2 was observed in the model ($1.77\mu M$ healthy; $2.80\mu M$ type 1 haemochromatosis), the up-regulation was slightly smaller than the change observed in vivo [@Robb2004Regulation]. This is due to the model having fixed extracellular transferrin bound iron concentration, in contrast to haemochromatosis where this concentration increases due to higher absorption in the intestine.

Type 3 haemochromatosis results in similar phenotype as type 1 haemochromatosis, however the mutation is found in the TfR2 gene as opposed to HFE. A virtual TfR2 knockdown mutation was performed by decreasing 100-fold the rate constant of synthesis of TfR2 from the model. Model results were then compared with the findings of Chua [*et al.*]{} [@Chua2010Iron]. The simulation showed a steady state decrease of liver TfR1 from $0.29\mu M$ to $0.19\mu M$ with TfR2 knockdown. This is supported by an approximate halving of TfR1 levels in TfR2 mutant mice [@Chua2010Iron]. An increase in hepcidin and consequent decrease in ferroportin as seen in mice was matched by the simulation.

An iron overload phenotype with increased intracellular iron is not recreated by the model of the TfR2 mutant. This is, 