Fanconi's anemia (FA) is a genetic disease characterized by increased chromosome instability associated with congenital malformations, progressive pancytopenia and increased susceptibility to cancer. FA lymphocytes have an accelerated shortening of telomeres, but the molecular mechanisms involved are unclear. In February Human Molecular Genetics, Elsa Callén and colleagues from Vall d'Hebron Hospital, Barcelona, Spain, show that both telomere breakage and replicative shortening account for the in vivo telomere shortening seen in FA peripheral lymphocytes.