NEU1 and sialidosis: Using the appropriate molecular and biochemical context is also fundamental for deciphering new cell type-specific pathogenic mechanisms: Seol et al. provided the first evidence that lysosomal sialidase gene (NEU1) deficiency alters, not only lysosomal dynamics, but also autophagic activity [25]; Odaka et al. revealed defective presynaptic exocytosis and excessive enhancement of AMPA-evoked Ca2+ influx in sialidosis [26]; and Liedtke et al. uncovered possible differences between NPC1 and NPC2 that showed indistinguishable biochemical phenotypes [28], among others.