Excess parenteral (non-ingested) iron supplements, such as what can acutely happen in iron poisoning
Excess dietary iron
Some disorders do not normally cause haemochromatosis on their own, but may do so in the presence of other predisposing factors. These include cirrhosis (especially related to alcohol use disorder), steatohepatitis of any cause, porphyria cutanea tarda, prolonged haemodialysis, and post-portacaval shunting

Diagnosis
There are several methods available for diagnosing and monitoring iron loading. Blood test
Blood tests are usually the first test if there is a clinical suspicion of iron overload. Serum ferritin testing is a low-cost, readily available, and minimally invasive method for assessing body iron stores. However, the major problem with using it as an indicator of iron overload is that it can be elevated in a variety of other medical conditions including infection, inflammation, fever, liver disease, kidney disease, and cancer. Also, total iron binding capacity may be low, but can also be normal. In males and postmenopausal females, normal range of serum ferritin is between 12 and 300 ng/mL (670 pmol/L) . In premenopausal females, normal range of serum ferritin is between 12 and 150 or 200 ng/mL (330 or 440 pmol/L). If the person is showing the symptoms, they may need to be tested more than once throughout their lives as a precaution, most commonly in women after menopause. Transferrin saturation is a more specific test. Genetics
DNA/screening: the current standard of practice in diagnosis of haemochromatosis, places emphasis on genetic testing.
conclude that residues 88 to 109 of the second EGF domain mediate binding to platelets and assembly of the factor X activating complex.The structures of all four domains have been solved. A structure of the two EGF domains and the trypsin-like domain was determined for the pig protein. The structure of the Gla domain, which is responsible for Ca(II)-dependent phospholipid binding, was also determined by NMR.Several structures of super active mutants have been solved, which reveal the nature of factor IX activation by other proteins in the clotting cascade. Genetics
The gene for factor IX is located on the X chromosome (Xq27.1-q27.2) and is therefore X-linked recessive: mutations in this gene affect males much more frequently than females. At least 534 disease-causing mutations in this gene have been discovered. The F9 gene was first cloned in 1982 by Kotoku Kurachi and Earl Davie.Polly, a transgenic cloned Poll Dorset sheep carrying the gene for factor IX, was produced by Dr Ian Wilmut at the Roslin Institute in 1997. Role in disease
Deficiency of factor IX causes Christmas disease (hemophilia B). Over 3000 variants of factor IX have been described, affecting 73% of the 461 residues; some cause no symptoms, but many lead to a significant bleeding disorder. The original Christmas disease mutation was identified by sequencing of Christmas DNA, revealing a mutation which changed a cysteine to a serine.Recombinant factor IX is used to treat Christmas disease.