Furthermore, dysregulated redox homeostasis driven by elevated Nox4 derived ROS signaling underlies fibroblast-to-myofibroblast differentiation in the diseased prostatic stroma, indicating the potential clinical value of Nox4 inhibitors in preventing the functional pathogenic changes of stromal cells in benign prostate hyperplasia (BPH) and prostate carcinoma [6]. The gene discussed is NOX4; the disease is prostate carcinoma.