As these fuels may act as oncometabolites in cancer cells, it is conceivable to hypothesize that the O2-independent regulation of HIF-1α by GPER may result from the activation of the glycolytic pathway and the subsequent production of pyruvate and lactate, which are known to stabilize HIF-1α in normoxia [194,195,196], generating a condition known as pseudo-hypoxia [158]. Here, GPER1 is linked to cancer.