Moreover, the loss of function of the other components of thestructure-specific endonuclease heterodimers MUS81-EME1 (and possibly also EME2),XPF-ERCC1 and SLX4-SLX1 could also be associated with patients with an FA-likephenotype, although, for the moment, their potential mutations are associated witheither lethal or extremely strong clinical phenotypes that probably preclude thepossibility of their assignment to FA. The gene discussed is ERCC1; the disease is Friedreich ataxia.