While other sialidases also may contribute to the bypass pathway, it is important to note that transfection of Neu4 in cultured fibroblasts from patients with sialidosis or galactosialidosis and of neuroglia cells from a patient with Tay-Sachs disease resulted in increased sialidase activity and normalization of lysosomal morphology [10], [11]. The gene discussed is NEU4; the disease is galactosialidosis.