Nowadays, it is well establishedthat DUOX2 is the NOX isoform that sustains TH production, since mutations inDuox2, but not in Duox1, are associatedwith congenital hypothyroidism in mice, and mice deficient inDuox2, but not Duox1, are hypothyroid(Johnson et al.,2007; Grasberger, 2010).However, DUOX1 seems to be able to compensate DUOX2 activity, since patientswith complete inactivation of both alleles of DUOX2 presented partial andtransient hypothyroidism (Maruo etal., 2008; Hosteet al., 2010). Here, DUOX1 is linked to congenital hypothyroidism.