NFKB1 and nasopharyngeal carcinoma: Kuang et al. [43] demonstrated that the activation of NF-κB is essential for cisplatin-resistance, as reflected by up-regulated expression of anti-apoptosis proteins and attenuated cell death in cisplatin-resistant nasopharyngeal carcinoma cells compared to the cisplatin-sensitive cells, thus suggesting that combining cisplatin with a NF-κB inhibitor, such as PG2, may help enhance the therapeutic efficacy of cisplatin; thus, the significance of our data shows that PG2 suppresses the nuclear accumulation of NF-κB and synergistically enhances the anticancer effect of cisplatin (Figure 5).