In support of this idea, Fancc-/-+Sod1-/- mice with the latter gene mutation promoting oxidative stress show a much improved FA disease modeling over the monogenic Fanc model53, as do Fancd2-/-+Aldh2-/- mice15 demonstrating the broader importance of polygenic mutations in FA development beyond Brca2 and Rad51c. Here, RAD51C is linked to Friedreich ataxia.