Our current reports indicate this is due to defective trafficking of late endosomes to lysosomes, with concomitant homotypic fusion on the afflicted vesicular compartments [five]. The defect in lysosome-directed trafficking also affects autophagic flux, with resultant accumulation of autophagosomes [5]. In the end, the integrity on the mobile membrane is https://williamo787nfx9.wikicorrespondent.com/user