Similarly to colon cancer cells [45], hypoxic UBC cells, in the absence of functional Hypoxia-Inducible Factor 1-alpha (HIF1α) (a key regulator of hypoxia response) pathway, could adapt their energy metabolism via the upregulation of creatine metabolism (and synthesis), thus opening a new chemotherapeutic window for metastatic UBC targeting and management in the clinic. This evidence concerns the gene HIF1A and colonic neoplasm.