In recent times, an attenuated G2 checkpoint phenotype, characterized by low levels of CHK1 (NP_001107594.1) and p53 (NP_000537.3), absence of the G2 phase arrest, and arrival to metaphase with a large number of MMC-induced CAs has been described in cells from adult FA individuals [31]. Here, CHEK1 is linked to Friedreich ataxia.