In our opinion, the main hypotheses to be tested are: (i) at the transcriptional level, a normoxic activation of HIF-1 by intracellular pyruvate (as previously reported for oxidative cancer cells and endothelial cells [36]), and (ii) postranscriptionally, MCT4 protein stabilization through increased interaction with CD147/basigin and/or reduced degradation kinetics. The gene discussed is SLC16A3; the disease is cancer.