Moreover, it has been reported that exogenous HOTAIR overexpression in ovarian cancer cells significantly promoted cisplatin resistance by regulating the Wnt/β-catenin signaling pathway as well as the NF-κB-HOTAIR axis, indicating that HOTAIR may act as a regulator of cisplatin resistance (Li J. et al., 2016; Ozes et al., 2016). The gene discussed is NFKB1; the disease is ovarian cancer.