Our observations of altered MAPK and PI3K/Akt signaling in DM1 suggest dysregulation of pathways like GSK3β-CUGBP1 (Lutz et al., 2023), which may contribute to disease pathophysiology and provide potential avenues for future therapeutic strategies targeting both the molecular underpinnings and clinical progression of DM1. Here, AKT1 is linked to myotonic dystrophy type 1.