Likewise, while it seems reasonable to try to alleviate the irreversible permanent PG storage in secondary glycogen storage disease (SGSD) by using molecules that bind to the lysosomal membrane protein (LAMP-1) [26] in order to enhance autophagic glycogen catabolism [27], this would not be recommended for a non-progressive and reversible lesion such as drug-induced GGG. Here, LAMP1 is linked to Glycogen storage disease due to glycogenin deficiency.