The advent of CRISPR/Cas9 genome editing has opened the potential for efficient correction of disease-causing genetic mutations in patient-derived HSCs, including the A-to-T base mutation within codon 6 of the HBB gene in SCD patients that is responsible for the mutant HbS allele and the resulting glutamic acid to valine (E6V) amino acid substitution within beta-globin3–5. The gene discussed is HBB; the disease is Schnyder corneal dystrophy.