A comparison of gene expression patterns in patients with DMD and aging skeletal muscle identified cell cycle dysregulation in addition to fibrosis.[15] Increase in p21 mRNA levels has been previously demonstrated in fibroblasts from a patient with severe CM.[16] p21 activation is also correlated with the terminal cell cycle arrest of myocytes.[17] Dux4 overexpression, as is seen in facioscapulohumeral dystrophy, leads to increased p21.[18] This was mediated by Dux4 recruitment of Sp1 to the promoter region of p21. The gene discussed is CDKN1A; the disease is Duchenne muscular dystrophy.