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). The gene discussed is RAD51C; the disease is Friedreich ataxia.