Our current studies reveal this is due to defective trafficking of late endosomes to lysosomes, with concomitant homotypic fusion with the affected vesicular compartments [five]. The defect in lysosome-directed trafficking also has an effect on autophagic flux, with resultant accumulation of autophagosomes [5]. In the end, the integrity with the https://michaelc196xbg0.wikipowell.com/user