Excess iodine in HT patients mediates tissue injury by an array of mechanisms, the most important of which are (1) chemokine-mediated lymphocytic infiltration in the thyroid parenchyma; (2) increased thyroglobulin iodination and induction of NF-κB -dependent expression of proinflammatory markers such as ICAM-1 and IL-6; (3) increased polyunsaturated fatty acid auto-oxidation followed by the generation of an array of aldehydes such as 4-hydroxy-2-alkenals (4-HNE). The gene discussed is ICAM1; the disease is hematocrit.