In support of this notion, more than 50% of individuals with CH associated with DUOX2 or DUOXA2 mutations exhibit TCH, including those harbouring biallelic-truncating DUOX2 mutations, which abolish the H2O2-generating domains and presumably abrogate DUOX2 activity completely (27, 47). Here, DUOXA2 is linked to cyclic hematopoiesis.