While in cell lines, we were able to demonstrate the overexpression of HIF1A compared to non-tumor cells and, in turn, its expression pattern was similar to that observed in HOTAIR, establishing a positive correlation, which could be associated with the constitutive activation of HIF-1α described by our group in cervical cancer cells, as well as by the induction of HOTAIR through the binding of HIF1A to its promoter [40,41]. The gene discussed is HOTAIR; the disease is neoplasm.