Liu et al. report in Nature Genetics a gene-editing strategy for severe α-thalassemia based on reactivating embryonic ζ-globin. The authors identified regulatory elements responsible for silencing the HBZ gene after early development and disrupted these elements to restore ζ-globin expression. In patient-derived erythroid cells from HbH disease and Hb Bart’s hydrops fetalis syndrome, ζ-globin production reached levels with potential therapeutic value. The approach improved survival in a severe mouse model. (https://www.nature.com/articles/s41588-026-02770-0)