Nelson et al. reported widespread alterations in the autophagy-lysosome pathway associated to neurodegenerative phenotype in the brain of a mouse model of alpha-galactosidase A deficiency: notably, microtubule-associated protein light chain 3 (LC3), a marker of autophagic vacuoles, was substantially increased in multiple brain regions, and likewise, lysosome-associated membrane protein LAMP-1, a lysosomal marker, was increased also in vascular endothelial cells, suggesting an aberrant autophagy process in FD [27]. Here, GLA is linked to Fabry disease.