Neutrophils generate reactive oxygen species (ROS), primarily to kill phagocytosed bacterial pathogens, via ATP-dependent NOX2 and mitochondrial (mtROS) oxidative phosphorylation [13, 25, 44]. We tested the impact of host Nox2 depletion on bone metastatic prostate cancer growth in vivo using an intratibial metastasis model of mouse RM1 prostate cancer cells. The gene discussed is CYBB; the disease is Familial prostate cancer.