So our HFE mutations prevent increased Alk3 protein levels on the cell surface of hepatocytes (liver cells). Alk3 is critical to hepcidin expression. Without hepcidin, the body continuously recycles and absorbs iron leading to iron overload.
This is a significant finding because hepcidin is a huge and complex molecule which is very difficult to whereas Alk3 may be easier to manipulate pharmacologically.
For others that may be interested in keeping up with Dr. Muckenthaler, here is a handy link to her most recent publications.