Downstream sequelae include induction of a DNA damage response evident by accumulation of 53BP1, p53, and p21 proteins, mitochondrial demise, and metabolic failure in DMD hiPSC-CMs, in agreement with mTRG4 mouse models of aging (Sahin et al., 2011) and the DMD mouse model with “humanized” telomeres (mdx4cv/mTRG2) (Chang et al., 2016). The gene discussed is TP53; the disease is Duchenne muscular dystrophy.