Our new reports show this is due to defective trafficking of late endosomes to lysosomes, with concomitant homotypic fusion with the impacted vesicular compartments [5]. The defect in lysosome-directed trafficking also influences autophagic flux, with resultant accumulation of autophagosomes [five]. Ultimately, the integrity with the mobile membrane is compromised and https://alvav110vof2.onzeblog.com/profile