Exposure of renal tubular epithelial cells to low-dose chemical NO and iNOS-derived NO, similar to CO, induces the accumulation of HIF-1α under normal O2 conditions (47); however, a high dose of NO donor cannot display the same result in the epithelial cells (47) and abrogates hypoxia-induced HIF-1α accumulation in hepatoma and neuronal cells (48). This evidence concerns the gene HIF1A and hepatocellular carcinoma.