Busulfan (Bu) combined with cyclophosphamide (Cy) is commonly used as a myeloablative conditioning regimen for allogeneic hematopoietic cell transplantation (allo-HCT). There is inter-individual variability of Bu pharmacokinetics (PK) and hence in toxicity and efficacy. The introduction of therapeutic drug monitoring (TDM) of Bu has decreased toxicity of the regimen. Hepatic metabolism of Bu is mediated through Glutathione-S-Transferases (GSTs), mainlyGSTA1. Patients withGSTA1*A variants are considered normal metabolizers andGSTA1*B corresponds to poor metabolism, defined by nucleotide changes at −52 or −69 locus inGSTA1promoter region. The aim of the study was to explore the correlation betweenGSTA1polymorphisms and Bu-PK in 60 adult patients receiving an allo-HCT in the BuCyBu clinical study (ClinicalTrials.gov I, ID NCT01779882) comparing the sequence BuCy to CyBu. DNA samples prior to conditioning were genotyped for candidate variants at −52 (rs3957356) and −69 (rs3957357) loci in theGSTA1 promoter. Thirty-three % of patients wereGSTA1*A*A, 49%GSTA1*A*B and 18%GSTA1*B*B. InGSTA1*A*A patients, median Bu-AUC was 3.6 ± 0.7 mg*h/L, inGSTA1*A*B 4.5 ± 1.6 and inGSTA1*B*B 4.9 ± 1.4 (AUC 35% higher thanGSTA1*A*A,p= 0.03), with a similar significant correlation with Bu-clearance (p= 0.04). The correlation betweenGSTA1polymorphism and AUC remained significant in multivariate linear regression analysis. There was a trend for lower non-relapse mortality (NRM) in patients with low AUC. We could not demonstrate a correlation betweenGSTA1polymorphisms and NRM, acute graft-versus-host disease (aGvHD) in this small cohort, but there is a trend of higher aGvHD incidence inGSTA1*B*B patients.