To investigate the role of the NF-κB signaling pathway in regulating CD44 expression in BCa cells, bladder cancer cells were treated with TNFα (an activator of NF-κB signaling) after ITPR3 knockdown, and we found that TNFα reversed the expression of P-NFκB and CD44 simultaneously suppressed by ITPR3 knockdown, which indicated that activation of the NF-κB signaling pathway antagonized the low expression of CD44 caused by ITPR3 knockdown and that NF-κB functioned upstream of CD44 in BCa cells (Fig. 7f). This evidence concerns the gene NFKB1 and urinary bladder carcinoma.