HIF-1α also acts as a transcriptional mediator of tissue hypoxia; HIF-1α is hyperactivated in conditions of prolonged anoxia as a consequence of possible adaptation to tumour microenvironment factors, the reduction in mitochondrial respiration in low-oxygen environments, and the subsequent Warburg effect, conditions that alternate with the control of ROS and therefore the modulation of oxidative stress. Here, HIF1A is linked to neoplasm.