Based on our results employing solely human primary hepatocytes and precision-cut slices of healthy human liver tissues versus malignant human liver tissues, it seems feasible that fructose-induced depletion of ATP represents a general way of protecting the human liver from unwanted energy-dependent cell death induced by TNF in IHP-based local cancer therapy whereby the sensitivity of liver tumors towards cytotoxic therapies is retained. The gene discussed is TNF; the disease is cancer.