GBA1 and Parkinson disease: Several knock-in (KI) models harboring GD/PD-associated GBA1 mutations (e.g., Gba1+/L444P, Gba1+/D409V, Gba1+/N370S) mimic the heterozygous “risk-carrier” state, exhibiting 20–40% reductions in GCase activity and modest GlcCer/GlcSph accumulation, with only subtle lysosomal and oxidative stress in the absence of overt neurodegeneration or motor symptoms.