One of the important questions related to the benefits of TG treatments in congenital DM1 (CDM1) and DM1 is whether TG corrects muscle pathology mainly via the GSK3β-cyclin D3-CUGBP1 pathway or whether TG normalizes other GSK3β-dependent substrates in HSALR muscle. This evidence concerns the gene GSK3B and myotonic dystrophy type 1.