Emerging evidence shows that PCa-associated exosomes shuttle inactive TGFβ1, which induces a pro-tumorigenic phenotype differentiation of normal fibroblasts to CAFs via Mothers against Decapentaplegic Homolog 1 (SMAD)-dependent and -independent signaling pathways [131,132,133,134,135]. The gene discussed is TGFB1; the disease is posterior cortical atrophy.