Presumably, exhaustion of HSCs in the Ercc1 mutant is largely caused by its replication‐associated cross‐link repair defect, as in Fanconi's anaemia (FA), in line with the notion that defects in the ERCC1 partner XPF can cause FA (Bogliolo et al., 2013; Kuraoka et al., 2000). The gene discussed is ERCC4; the disease is Friedreich ataxia.