a mathematical model and computer simulation. The model was constructed mostly based on [*in vitro*]{} biochemical data, such as protein complex dissociation constants. The model was then validated by comparison with experimental data from multiple physiological studies at both steady state and during dynamic responses. Where quantitative data were available the model matched these well and also qualitatively recreated many findings from clinical and experimental investigations. The simulation accurately modelled the highly prevalent iron disorder haemochromatosis. The disease state was simulated through altering a single parameter of the model and showed quantitatively how an iron overload phenotype occurs in patients with a HFE mutation.

Due to the limited availability of quantitative clinical data on human iron metabolism, various other data sources, particularly from [*in vitro*]{} experiments and animal models, were integrated for the parameterisation of this model. This computational modelling effort constitutes a clinical translational approach, enabling data from multiple sources to improve our understanding of human iron metabolism. Several arguments could be raised to cast doubt on this approach, such as the the failure of [*in vitro*]{} conditions to mimic those [*in vivo*]{} or the difference between animal models and humans. This means that this type of data integration 