In these settings, genetic ascertainment can inform appropriate counselling for disorders where multisystem involvement is anticipated (e.g., NKX2‐1, FOXE1, GLIS3, and Pendrin mutations), or permit tailored treatment, with withdrawal of levothyroxine in childhood if CH is likely to be transient (e.g., DUOX2/DUOXA2‐mediated CH) or in individuals with hyperthyrotropinaemia due to heterozygous TSHR mutations who may not require treatment at all.1, 8, 10. The gene discussed is TSHR; the disease is cyclic hematopoiesis.