This is particularly important as mutations in both DUOX1 and DUOX2 in humans have been associated with a more severe form of CH (Aycan et al., 2017), suggesting that DUOX1, while normally playing a minor role in TH synthesis in humans, does partially compensate for the loss of DUOX2 in humans. The gene discussed is DUOX2; the disease is cyclic hematopoiesis.