Moreover, GOLPH3L overexpression enhanced cisplatin resistance, but GOLPH3L silencing restored the sensitivity of ovarian cancer cells to cisplatin by regulation of the NF-κB signaling pathway, suggesting that GOLPH3L contributes to ovarian cancer progression and thereby represents a novel target for overcoming cisplatin resistance in ovarian cancer therapy. The gene discussed is NFKB1; the disease is ovarian cancer.