In all, our findings also implicate that besides direct targeting eNOS and also its downstream NO-mediated signaling effectors (such sGC and PKG), targeting the upstream regulators of eNOS could be an alternative approach to attenuate the activated eNOS-NO signaling in PCSCs in order to suppress their stemness or growth in prostate cancer. The gene discussed is NOS3; the disease is Familial prostate cancer.