By promoting androgen-independent transcription of the KLK3 gene via NF-kB and intratumor sequestration of PSA shaping the tumor microenvironment, sterile inflammation induced by PCa cells secretion of TRPM8 RNA in EVs may introduce a further layer of complexity in the evaluation of PSA levels or PSA derivatives affecting our ability to monitor the disease (PSA doubling time, PSA velocity, biochemical recurrence, biochemical response/progression). The gene discussed is NFKB1; the disease is neoplasm.