Broadly speaking, ID can be attributed to the factors related to HF per se (e.g. malabsorption due to venous congestion, impaired nutrition, reduced intracellular uptake of iron due to reduced cellular TfR1, iron sequestration associated with chronic inflammation accompanying HF, and intracellular abnormalities of iron handing in cardiomyocytes) or to the factors related to co-morbidities and concomitant medications (e.g. gastrointestinal or genitourinary blood loss related to the use of antiplatelet drugs and/or oral anticoagulants)2. This evidence concerns the gene TFRC and hydrops fetalis.