Tumor progression is well known to be associated with hypoxia, which itself gives rise to enhanced stabilization of the master regulator HIF-1α and also to an augmented release of ROS, caused by an increased leakage of the mitochondrial electron transport chain. Due to its high O₂ affinity, Mb may serve as an O₂ store and facilitate O₂ transport from capillaries to mitochondria even under conditions of limited O₂ availability. As a consequence, the ectopic expression of Mb within cancer cells carried out by Galluzzo et al. (4) leads to an improved O₂ supply to the tumor, as reflected by the enhanced tissue O₂ partial pressure (pO₂) reported in this study. Additionally, Mb can reduce oxidative and nitrosative stress in cancer cells by detoxification of ROS to water and of NO radicals (NO•) to nitrate (NO₃^–), respectively. Together, these result in an environment of enhanced aerobic mitochondrial respiration and reduced levels of free radicals, favoring efficient degradation of HIF-1α, a key player in the progression of tumor metabolism to a more aggressive phenotype (15). As demonstrated by Galluzzo et al. (4), the metabolic environment created by the presence of Mb in cancer cells furthermore implicates cell differentiation, a reduction in vascular abnormalities, and a reduced selection of aggressive cells, which, in turn, retards tumor growth and metastatic spread.