Approximately 15–20% of CH cases result from thyroid dyshormonogenesis (DH) caused by mutations in thyroid hormone synthesis pathway genes, including those involved in hormone precursor production (thyroglobulin (TG)) [2], iodine transportation across the basal membrane (solute carrier family 5 member 5 (SLC5A5) [3], solute carrier family 26 member 4 (SLC26A4) [4]), thyroglobulin modification (thyroid peroxidase (TPO) [5], dual oxidase 2 gene (DUOX2) [6], and dual oxidase maturation factor 2 (DUOXA2) [7]), and iodine recycling in the thyroid (iodotyrosine deiodinase (IYD)) [8]. Here, DUOX2 is linked to familial thyroid dyshormonogenesis.