Because LDHA silencing can alter cancer cell metabolism from glycolysis to mitochondrial respiration (through preferring the entry of pyruvate into mitochondria), lack of LDHA enhances oxygen consumption (in both p53+/+ and p53 -/- cancer cells), which results in elevated level of mitochondrial reactive oxygen species (ROS) (~2.3 fold; p < 0.001 in LDHA deficient HCCLM3 hepatocellular carcinoma cells compared to control cells) [67,69,70,71]. This evidence concerns the gene TP53 and hepatocellular carcinoma.