Known mechanisms affecting NRF2 activity independently of its levels include changes in the levels of its binding partners, such as the small musculoaponeurotic fibrosarcoma (sMAF) factors, or changes in NRF2 subcellular localization, as occurs in Hutchinson-Gilford progeria syndrome, where progerin, a lamin A mutant, retains NRF2 at the nuclear periphery [53]. Here, NFE2L2 is linked to Hutchinson-Gilford progeria syndrome.