A PKG inhibitor could re‐establish NF‐κB phosphorylation in CD8+ T cells and STAT5 phosphorylation and CCND1 expression in BECs, and restore BEC proliferation enhanced by CD8+ T cells, thereby implicating cGMP/PKG signaling in BPH pathogenesis. This evidence concerns the gene PRKG1 and benign prostatic hyperplasia.