Since the TG-GSK3β pathway reduces the mutant DMPK mRNA in human DM1 cells and CUG-containing transcripts in HSALR muscle [18], the increased levels of active GSK3β in PBMCs in DM1 patients could be used as one of the potential biomarkers to monitor the effects of these therapeutics. This evidence concerns the gene DMPK and myotonic dystrophy type 1.