Some studies reported that both DMPK± and DMPK-/- mice shown abnormal cardiac conduction (Berul et al., 1999, 2000), and homozygous deletion also exhibited skeletal myopathy and muscle weakness (Reddy et al., 1996), while other findings countered that the administration of DMPK-targeting ASOs with heterozygous deletion did not influence the normal cardiac or muscle function in mice, thereby supporting the feasibility and safety of ASOs usage in DM1 (Carrell et al., 2016). This evidence concerns the gene DMPK and myotonic dystrophy type 1.