The success of the treosulfan-based conditioning regimen in patients with β-thalassemia undergoing hematopoietic cell transplantation (HCT) is limited due to several complications, such as mixed chimerism and graft rejection. Researchers previously found that polymorphisms in the NQO1 or glutathione S-transferase A1 (GSTA1) genes had an impact on treosulfan pharmacokinetics, which then impacted related toxicities after HCT.