Two routes for the methylation of homocysteine to methionine, depending either on betaine or folate cofactor as methyl donor, were studied in liver and kidneys of normal and Ehrlich ascites carcinoma-bearing mice at various stages of their postnatal development. Distinct age-dependence in the activities of betaine methyltransferase, methylenetetrahydrofolate reductase and methionine synthase were found both in normal and tumour-bearing mice. Independent of the levels of enzyme activity in healthy mice, the tumour activated one route of methionine formation only, namely that utilizing methyltetrahydrofolate as the methyl donor. This effect was observed in host liver exclusively. No host age-related changes were found in Ehrlich ascites carcinoma growth.