Because NOX4 has the capacity to oxidize the substrates NADPH or NADH to NADP+ or NAD+(ref. 15), we posited that NOX4 may function as a compensatory mechanism and accelerates NAD+ and NADP+ circulation to sustain cellular glycolysis and pentose phosphate pathway activity in mitochondria-defective pancreatic cancer cells. The gene discussed is NOX4; the disease is familial pancreatic carcinoma.