GBA3 is a cytosolic neutral β-glucosidase with broad substrate specificity involved in glycosphingolipid catabolism 1. It possesses glucosylceramidase activity in vitro, though this activity is relatively low and its physiological significance remains unclear 2. GBA3 hydrolyzes galactosylceramides, glucosylsphingosines, and galactosylsphingosines, and can metabolize diverse dietary glycosides including xenobiotics and phytoestrogens 1. Additionally, GBA3 exhibits transxylosylase activity and may participate in cytosolic sialyl free N-glycan catabolism by stabilizing the sialidase NEU2 3. Notably, GBA3 is a polymorphic pseudogene in humans with a truncated allele that is inactivating, and the gene has undergone repeated pseudogenization events across mammalian evolution, possibly linked to dietary adaptations 4. Unlike GBA1 (deficiency causes Gaucher disease), GBA3 deficiency does not influence type 1 Gaucher disease manifestation 2. However, decreased GBA3 expression correlates with poor prognosis in hepatocellular carcinoma patients, suggesting potential tumor-suppressive functions 5. GBA3 is primarily expressed in kidney, liver, spleen, intestine, and lymphocytes 1.