However, because GluSph levels were numerically higher in carriers with PD compared with carriers without PD (0.82 ± 0.24 versus 0.73 ± 0.20), and in noncarriers with PD compared with controls (0.50 ± 0.14 versus 0.48 ± 0.14), we posit that a larger cohort of GBA mutation carriers and noncarriers will be needed to investigate whether GluSph levels are associated PD status. The gene discussed is GBA1; the disease is Parkinson disease.