Only animals with combined inactivation of aldehyde catabolism (through Aldh2 knockout—ALDH2, the mitochondrial aldehyde dehydrogenase that is primarily responsible for oxidation of acetaldehyde) and the Fanconi anemia DNA-repair pathway (Fancd2 knockout) display susceptibility to the toxic effects of ethanol; the Fanconi anemia pathway prevents aldehyde lesions from degenerating into DSBs [57]. This evidence concerns the gene FANCD2 and Fanconi anemia.