Defects in the Fanconi anemia (FA) pathway and mutations in ataxia telangiectasia (ATM), ataxia telangiectasia and Rad3-related (ATR) or phosphatase and tensin homolog (PTEN) are suggested to contribute to the HR-deficient phenotype [10, 15, 19, 21, 31, 32]. The gene discussed is PTEN; the disease is telangiectasis.