HOTAIR is overexpressed in ovarian cancer, which induces NF-κB activation and the subsequent secretion of IL-6 (an NF-κB downstream molecule that activates STAT3, also playing a critical role in reprogramming the TME [164]) by suppressing Iκ-Bα (an NF-κB inhibitor). This evidence concerns the gene NFKB1 and ovarian carcinoma.