AN insight into the biochemical strategy of cancer cells has been achieved by the conceptual and experimental approach provided by the molecular correlation concept^1,2. Studies carried out using this approach with model systems of rat hepatomas and kidney tumours of different growth rates revealed a biochemical imbalance in cancer cells, which manifested itself in progressive changes in activities of key enzymes and overall metabolic pathways that correlated with tumour growth rate^1,2. Some of these biochemical alterations have been shown to apply to human primary liver³ and kidney⁴ carcinomas. Those alterations in gene expression that are linked to the increase in the expression of malignancy are manifested in the increased activities of key glycolytic-, purine-, pyrimidine-, DNA- and polyamine-synthesising enzymes^1–8. Concurrently, decreases occur in the activities of the key enzymes of gluconeogenesis, purine and pyrimidine catabolism and of the urea cycle^1–5,9,10. In addition to such a progression-linked (growth-rate-linked) metabolic imbalance, the reprogramming of gene expression in cancer cells entails transformation-linked alterations that are present in all hepatomas irrespective of growth rate or extent of differentiation^1,2,11–15.Here we report that CTP synthetase (UTP:L-glutamine amido ligase, EC 6.3.4.2) increased in all the hepatomas examined, the activity being highest in the rapidly growing tumours. Thus, in liver neoplasia the activity of this enzyme is both transformation- and progression-linked. CTP synthetase activity was also markedly increased in transplantable kidney tumours in the rat and in primary renal cell carcinomas in man.