To do this, Fx inhibited cisplatin-induced expressions of NF-κB, excision repair cross complementation 1 (ERCC1) and thymidine phosphorylase (TP) [57], leading to improvement of chemotherapeutic efficacy of cisplatin by activation of apoptosis, inhibition of DNA repair and promoting tumour regression. Here, NFKB1 is linked to neoplasm.