For example, Panduri et al. [33] found that overexpression of mitochondria-targeted OGG1 could prevent oxidant-induced mitochondrial dysfunction in human lung adenocarcinoma cells by preserving mitochondrial aconitase, inactivation of which is known to promote superoxide radical from its (4Fe-4S)2+ center. This evidence concerns the gene OGG1 and lung adenocarcinoma.