Indeed, one can envisage a scenario where alternating regimes are applied, based upon inhibition of nucleotide biosynthesis (leading to selection for tumour cells that elevate biosynthetic capacity and therefore elevate metabolic demand) followed by inhibition of the TCA cycle and AK2 (leading to tumour suppression due to lack of energetic support for the excessive metabolic demand). The gene discussed is AK2; the disease is neoplasm.