This suggests that SMAUG1 improves the activity of the CUGBP1-containing translational complexes that are dysfunctional in DM1, a hypothesis that is supported by data showing SMAUG1-mediated increased translation of the CUGBP1 translational target MRG15 in DM1 myoblasts. Here, SAMD4A is linked to myotonic dystrophy type 1.