FA individuals have defects in the molecular machinery of detection and repair of interstrand crosslinks (ICLs) and DNA double-strand breaks (DSBs), which are mostly due to the biallelic inheritance of recessive pathogenic variants in a subset of at least 20 FANC genes (FANCA, FANCC, FANCD1 (BRACA2), FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ (BRIP1), FANCL, FANCM, FANCN (PALB2), FANCO (RAD51C), FANCP (SLX4), FANC (ERCC4), FANCS (BRCA1), FANCT (UBE2T), FANCU (XRCC2), FANCV (MAD2L2), FANCW (RFWD3)) (Wang and Smogorzewska, 2015). This evidence concerns the gene MAD2L2 and Friedreich ataxia.