To the best of the authors' knowledge, expression levels of DUOX1/DUOXA1 and DUOX2/DUOXA2 have not been characterized in the early neonatal period, but if the expression and functional importance of DUOX2 were to increase relative to DUOX1 shortly after birth, this may result in decompensated hypothyroidism in cases harboring DUOX2/A2 mutations due to a failure of DUOX1 to compensate for the defect. This evidence concerns the gene DUOXA2 and hypothyroidism.