Whereas permanent CH is caused by a variety of genetic defects in addition to DUOX2 (e.g., TPO, TG, PAX8) as well as sporadic developmental abnormalities (e.g., ectopic thyroid gland), partial defects in the DUOX2 enzyme complex (DUOX2, DUOXA2) are the major known genetic risk factor for transient CH1,2,16–18. Here, DUOX2 is linked to cyclic hematopoiesis.