Importantly, reactivation of NRF2 activity in HGPS patient cells reverses progerin-associated nuclear aging defects, suggesting that progerin-dependent repression of NRF2-mediated antioxidant responses is a key factor underlying HGPS-type premature aging with potential relevance to chronological aging and UVA-induced photoaging. The gene discussed is LMNA; the disease is Hutchinson-Gilford progeria syndrome.