In this regard, we have recently showed, in the PCa setting, that tumor-derived interleukin-6 (IL6), via the secretion of soluble factors including metalloproteases, may itself activate normal fibroblasts and subsequently (i) induce epithelial-mesenchymal transition (EMT) in PCa cells, thus increasing their invasive capability, (ii) favor the expression of stemness markers, and (iii) support PCa growth and metastasis in vivo, as also observed for patient-derived CAFs [10]. The gene discussed is IL6; the disease is posterior cortical atrophy.