Defects in homologous-recombination repair can also be caused by loss of function of proteins other than BRCA1 and BRCA2, including the RAD51, ataxia telangiectasia mutated (ATM), ataxia telangiectasia and Rad3 related (ATR), and checkpoint kinase 1 and 2 homologue (CHK1 and CHK2) proteins, as well as components of the Fanconi's anemia repair pathway [44]. The gene discussed is ATR; the disease is Fanconi anemia.