HIF1A and neoplasm: RAS oncogene activation and oxidative stress that are attributed to overproduction of ROS induce the upregulation of cancer-associated fibroblasts MCT4 (HIF-1α) in the TME, leading to decreased mitochondria function and increased rates of glycolysis, with consequent production of L-Lactate and ketone bodies that are taken up by cancer cells as an energy source for oxidative phosphorylation, thereby realizing the “metabolic symbiosis” between tumour cells and adjacent cells (229).