In DM patients insulin resistance has been associated with aberrant splicing of the insulin receptor gene (INSR) due to a toxic effect of the CUG/CCUG-expanded repeats [10–11] that leads to a higher expression of the fetal isoform A (INSR-A, lacking exon 11) than the adult insulin-sensitive isoform B (INSR-B). Here, INSR is linked to Insulin resistance.