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. This evidence concerns the gene ERCC4 and Friedreich ataxia.