These results are consistent with those previously obtained in the same regeneration system by chronic exposure to paracrine FGF10 (15): induction of PIN and PCa was achieved (15), probably through Src activation, since Src is known to mediate FGF-signaling, while selective Src loss or inactivation inhibited FGF10-induced PIN and PCa (18). This evidence concerns the gene FGF10 and prostate intraepithelial neoplasia.