Given the spatial association of abundant stromal Nox4 expression with TGFβ‐expressing tumor foci in clinical PCa, these findings collectively provide a strong mechanistic rationale for therapeutic inhibition of Nox4 as a stromal‐targeted approach to complement current treatment strategies for PCa and restore dysregulated reciprocal stromal–epithelial interactions. The gene discussed is TGFB1; the disease is posterior cortical atrophy.