Although Fanca−/− and Fancc−/− mice do not demonstrate reduced numbers of HSCs as determined by flow cytometry analysis, they do have impaired proliferation of progenitors in vitro and show a decreased long-term repopulating ability of HSCs in competitive transplantation assays in vivo (Figure 1), which may be related to the development of BMF in FA patients [88–90]. Here, FANCC is linked to Friedreich ataxia.