Depending on the residual GAA enzyme activity, the disease either develops during the first months of life as the classic infantile Pompe disease (IOPD) [6], or later in life (childhood, adolescence or adulthood) with a milder phenotype known as late-onset Pompe disease (LOPD) [3]. Here, GAA is linked to glycogen storage disease due to acid maltase deficiency, late-onset.