Personalised medication of cancer, based on genomic analysis, predominates the fields of sci-ence and healthcare. Much attention is also paid to metabolic changes related to the disturb-ance of glucose metabolism in cancer known as the Warburg Effect: the excessive uptake of glucose and its conversion to lactate even in the presence of oxygen. We hypothesise that the unwanted clonal proliferation of cancer cells can best be prevented by lowering their energy generating capacity without hampering this process in normal tissues. Cancer is caused by overexpression of, or mutations in oncogenes. Their products are practically all dependent on ATP for their function, but drugs interfering with their expression may affect comparable pro-cesses in healthy cells. This lack of specificity applies also to current metabolic and immuno-therapeutic approaches to fight cancer. For this reason, both strategies are prone to side ef-fects. In our opinion, carcinogenesis, caused by millions of different oncogene mutations, should be treated with a generalised rather than a personalised method. Carcinogenesis relies on mitochondrial oxidative phosphorylation for energy generation. Limitation of this capacity during clonal expansion of cancer cells by the antibiotic doxycycline offers an attractive ther-apeutic strategy. Early detection with a general tumour marker, is desirable.