In contrast, the phenotype was associated with the following abnormalities: (i) a predominant expression of immature splice products of genes involved in Ca2+ transport and channeling, (see Figure 3); (ii) significantly reduced levels of RyR1 protein, that decreased progressively from T10 to T15 in DM1 myotubes (Figure 4); (iii) induction of ER stress markers and a progressive membrane deformation that may induce disruption of triad junction and SR network (Figure 5, Figure 6) [30]. This evidence concerns the gene RYR1 and myotonic dystrophy type 1.