Chemotherapy‐induced DNA damage can increase WNT16B protein production in prostate fibroblasts, which is regulated by NF‐κB in B cells. WNT16B activates the classical Wnt program in tumour prostate epithelial cells in a paracrine manner, and Wnt signals can acquire mesenchymal cell properties via epithelial to mesenchymal transition, influencing epithelial cell migration and invasion behaviour, weakening the effect of cytotoxic chemotherapy in vivo, and promoting tumour cell survival and disease progression. Here, NFKB1 is linked to neoplasm.