do not successfully recreate the amplifying feedbacks that occur as a result of hepcidin expression controlling enterocyte iron export. To relieve this limitation, a more advanced model should include dietary iron uptake and the action of hepcidin on that process.

The model predicts a quasi-linear response to increasing pulses of serum iron, similar to what has been predicted for the erythropoietin system [@Becker2010Covering]. Our simulations display response of the transferrin receptors to pulses of extracellular transferrin-bound iron that is similar to the EPO-R response to EPO (Figure \[fig:TfRResponse\]). The integral of this response [*versus*]{} the iron sensed deviates very little from linearity in the range of physiological iron (Figure \[fig:EpoIron\]).

Computational models are research tools whose function is to allow for reasoning in a complex nonlinear system. The present model can be useful in terms of predicting properties of the liver iron system. These predictions form hypotheses that lead to new experiments. Their outcome will undoubtedly improve our knowledge and will also either confirm the accuracy of the model or refute it (in which case it then needs to be corrected). The present model and its results identified a number of predictions about liver iron regulation that should be investigated 