ATM and ataxia telangiectasia: Consistent observations of low numbers of N-nucleotides in the ends of the junctions in AT patients have also been reported previously both in human umbilical cord blood samples [40], neonatal mice [69, 70] as a result of low TdT activity during the fetal period, and antigen receptor development in TdT deficient mice [71], suggesting that low expression or dysfunction of TdT might be one of the downstream consequences of ATM deficiency.