Furthermore, mitochondrial defects and increased sensitivity of oxidative damage associated with PGC-1α repression were also observed in iPS-derived RPE cells from dry AMD patients (Golestaneh et al, 2016), suggesting that RPE metabolic alteration and oxidative damage act as key initiating events in the activation of the various degenerative mechanisms associated with AMD pathogenesis. The gene discussed is PPARGC1A; the disease is dry age related macular degeneration.