The prevailing view on BPH pathogenesis is that the cumulative effects of low‐level chronic stimulation of prostate cells by inflammatory secretions from the reactive stroma and infiltrated inflammatory cells promote excessive cell proliferation in aging prostate.27 Chemokines such as CXCL12 trigger infiltration of inflammatory cells to the prostate periacinar microenvironment. Here, CXCL12 is linked to benign prostatic hyperplasia.