However, the Neu4 and Neu3 KO mouse models do not develop massive lysosomal storage of any ganglioside or severe clinical phenotypes resembling those of the Glb1 KO mouse (model of GM1 gangliosidosis) or β-hexosaminidase deficient Hexb KO mouse (model of Sandhoff disease) [40, 75]. Here, NEU3 is linked to GM1 gangliosidosis.