First, transcriptomic and molecular studies identified the impairment of cell cycle control, cell division, and DNA replication and repair pathways together with higher p16INK4A, ARF, p53, and p21CIP1 in early-passage DM1 fibroblasts, indicative of cell cycle arrest and the initiation of the senescence process. This evidence concerns the gene CDKN2A and myotonic dystrophy type 1.