GAL and GM1 gangliosidosis: Our results also suggest that β-gal levels do not need to reach supraphysiological levels to promote substrate clearance; only very small amounts of β-gal augmentation are sufficient to mediate near-to-complete GM1 ganglioside substrate clearance, with as little as 14% of normal residual β-gal activity (Fig. 7A) being sufficient to maintain substrate clearance in GM1 gangliosidosis patient cells for up to 4 weeks following cellular uptake of rhβ-gal (Fig. 7D; see Fig. 7E for quantification).