The observations suggest that DUOX2/DUOXA2 mutations are a more common cause of borderline CH than anticipated and are consistent with the high frequency of defective iodide organification, likely due to underlying DUOX2/DUOXA2 defects, in cases with borderline CH (TSH <15 mIU/L), documented in a previous Italian study (7). This evidence concerns the gene DUOXA2 and cyclic hematopoiesis.