Consistent with this premise, myoblasts from FSHD-affected individuals are more susceptible to oxidative stress and show deregulation of MYOD (also known as MYOD1) (Winokur et al., 2003a,b), and differentiate into myotubes with abnormal morphology (Barro et al., 2008). The gene discussed is MYOD1; the disease is facioscapulohumeral muscular dystrophy.