In cells from NEU1 deficient mice, a model of the LSD sialidosis, impaired processing of sialic acids on LAMP1’s luminal domain prolongs its half-life and results in an increased number of LAMP1-decorated lysosomes docked at the PM, poised to engage in lysosomal exocytosis (Yogalingam et al., 2008; d’Azzo et al., 2015). This evidence concerns the gene LAMP1 and sialidosis.