It has been reported that the MCM8/9 complex participates in interstrand crosslink repair by functioning in RAD51-dependent HR repair downstream of the Fanconi anemia (FA) pathway (Nishimura et al, 2012), and Mcm8 and Mcm9 KO mice share the similar phenotype with FA-null mice of massive loss of proliferating PGCs (Luo and Schimenti, 2015; Yang et al, 2022). Here, MCM8 is linked to Friedreich ataxia.