The loss of cell cycle checkpoint controls caused by the inactivation of RB1 and TP53 increases susceptibility to DNA damage and the therapeutic targeting of central DDR mediators, such as PARP, checkpoint kinase 1 (CHK1), Ataxia telangiectasia and RAD3-related protein (ATR), Ataxia telangiectasia mutated (ATM), and WEE1, has been recently investigated in SCLC as it leads to tumour cells death by genomic instability. The gene discussed is ATR; the disease is neoplasm.