Briefly our results showed that: (i) ATR activity is important for DNA replication and diverse DDR pathways, (ii) CHK1 activity is important for replication checkpoint control and cell cycle regulation, (iii) the loss of Fanconi anemia (FA) pathway genes increases sensitivity to ATMi, ATRi and CHK1i, and 4) defects in apurinic/apyrimidinic site (AP)-site resolution or the single-strand break repair (SSBR) pathway sensitize cells to DNAPKi. The gene discussed is ATR; the disease is Friedreich ataxia.