A possible explanation is that in FD, FPN1 can still traffic to the cell membrane and export iron in enterocytes, but is unable to do so in Kupffer cells and macrophages indicating a different behavior of FPN1 activity between enterocytes and macrophages [269,274]. However, it seems that the pathophysiology of FD and HH4B are not that easy to be explained. This evidence concerns the gene SLC40A1 and Fabry disease.