A composition comprising a population of recombinant human acid α-glucosidase (rhGAA) molecules for use in the treatment of Pompe disease in a subject in need thereof, wherein the rhGAA molecules are produced from Chinese hamster ovary cells; wherein the rhGAA molecules comprise seven potential N-glycosylation sites; wherein the rhGAA molecules on average comprise 3-4 mannose-6-phosphate (M6P) residues; wherein the rhGAA molecules on average comprise at least about 0.5 mol bis-mannose-6-phosphate (bis-M6P) per mol of rhGAA at the first potential N-glycosylation site as determined using liquid chromatography-tandem mass spectrometry (LC-MS/MS); wherein the population of rhGAA molecules is administered concurrently or sequentially with a pharmacological chaperone, and wherein the pharmacological chaperone is miglustat or a pharmaceutically acceptable salt thereof; wherein the population of rhGAA molecules is administered intravenously at a dose of about 20 mg/kg and the miglustat or pharmaceutically acceptable salt thereof is administered orally at a dose of about 260 mg; and wherein (i) the subject is an ERT-switch patient, and, compared to baseline, the subject's pulmonary function, as measured by an upright forced vital capacity test, is stable or improved at six months after treatment; and/or (ii) the subject is an ambulatory ERT-switch patient and, compared to baseline, the subject's creatine kinase levels at six months after treatment are reduced at least 15%; and/or (iii) the subject is a nonambulatory ERT-switch patient and, compared to baseline, the subject's creatine kinase levels at six months after treatment are reduced at least 20%; and/or (iv) the subject is an ERT-switch patient, and, compared to baseline, the subject's levels of urine hexose tetrasaccharide at six months after treatment are reduced at least 35%. wherein the rhGAA molecules comprise seven potential N-glycosylation sites; wherein the rhGAA molecules on average comprise 3-4 mannose-6-phosphate (M6P) residues; wherein the rhGAA molecules on average comprise at least about 0.5 mol bis-mannose-6-phosphate (bis-M6P) per mol of rhGAA at the first potential N-glycosylation site as determined using liquid chromatography-tandem mass spectrometry (LC-MS/MS); wherein the population of rhGAA molecules is administered concurrently or sequentially with a pharmacological chaperone, and wherein the pharmacological chaperone is miglustat or a pharmaceutically acceptable salt thereof; wherein the population of rhGAA molecules is administered intravenously at a dose of about 20 mg/kg and the miglustat or pharmaceutically acceptable salt thereof is administered orally at a dose of about 260 mg; and wherein (i) the subject is an ERT-switch patient, and, compared to baseline, the subject's pulmonary function, as measured by an upright forced vital capacity test, is stable or improved at six months after treatment; and/or (ii) the subject is an ambulatory ERT-switch patient and, compared to baseline, the subject's creatine kinase levels at six months after treatment are reduced at least 15%; and/or (iii) the subject is a nonambulatory ERT-switch patient and, compared to baseline, the subject's creatine kinase levels at six months after treatment are reduced at least 20%; and/or (iv) the subject is an ERT-switch patient, and, compared to baseline, the subject's levels of urine hexose tetrasaccharide at six months after treatment are reduced at least 35%. (i) the subject is an ERT-switch patient, and, compared to baseline, the subject's pulmonary function, as measured by an upright forced vital capacity test, is stable or improved at six months after treatment; and/or (ii) the subject is an ambulatory ERT-switch patient and, compared to baseline, the subject's creatine kinase levels at six months after treatment are reduced at least 15%; and/or (iii) the subject is a nonambulatory ERT-switch patient and, compared to baseline, the subject's creatine kinase levels at six months after treatment are reduced at least 20%; and/or (iv) the subject is an ERT-switch patient, and, compared to baseline, the subject's levels of urine hexose tetrasaccharide at six months after treatment are reduced at least 35%.