Evidence suggests that IDA can precipitate IS through a triad of mechanisms: (i) Reduced hemoglobin levels precipitate a hypoxic condition; (ii) Hypoxia induces transferrin production via hypoxia-inducible factor-1, which then activates and interacts with thrombin/factor XIIa, impairing the activity of anticoagulant proteases, thus leading to a hypercoagulable state; (iii) IDA stimulates thrombin generation by platelets, resulting in thrombocytosis (51). This evidence concerns the gene TF and thrombocytosis disease.