Meanwhile, abnormal activation of NF-κB inflammatory signaling in tumor-associated stromal cells, such as myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs), up-regulates the production of pro-inflammatory cytokines, chemokines and growth factors, which facilitates the formation of immunosuppressive TME and promotes the growth and development of CRPC [59,60]. The gene discussed is NFKB1; the disease is neoplasm.