The molecular mechanisms driving fibroblast activation to the CAF phenotype remain poorly defined however several cytokines and growth factors (e.g., interleukins‐6, −8 and TGFβ) have been implicated.32 Taken together with reports that Nox4 is a direct transcriptional target of TGFβ/Smad signaling,33 the striking spatial association between expression of stromal Nox4 and TGFβ in tumor cells further implicate epithelial‐derived TGFβ as a crucial inducer of reactive stroma and underlying cause of elevated Nox4 expression in clinical PCa. Here, TGFB1 is linked to posterior cortical atrophy.