In our model, we found that IL6-JAK-STAT3 signalling and TNFA signalling via NFKB were positively enriched in both experimental groups, albeit that the IL6-JAK-STAT3 signalling may have been more strongly upregulated in the control group, while the interferon alpha response was exclusively enriched in the DM1 cells. This evidence concerns the gene STAT3 and myotonic dystrophy type 1.