if the recently described function of the DNA repair protein ataxia telangiectasia mutated (ATM) kinase and downstream activation of AMPK [50-56] is indeed secondary to metformin's ability to alter the carbon flow through the one carbon-related de novo maintenance of intracellular nucleotide pools, the ATM/AMPK tumor suppressive axis would be refractory to metformin's activating effects as long as the medium contains appropriate ready-formed thymidine and/or purines. This evidence concerns the gene ATM and neoplasm.