This cellular process is altered in several DM1 models, such as in Drosophila [5], human skeletal actin (HSA) LR mice, and human muscle cells [9], due to deregulation of the mammalian target of rapamycin (mTOR)/AKT [6,7] and AMP-activated protein kinase (AMPK) pathways, which alter a suitable cellular response upon starvation in DM1 mice [9]. The gene discussed is AKT1; the disease is myotonic dystrophy type 1.