The adult prostrate depends on androgens for its growth and function - its epithelium regresses when androgens are depleted. FGF signalling, through the FGF receptor FGFR2, has been implicated in mouse prostate development, but studies of FGFR2's role in prostate organogenesis have been hampered by the early embryonic death of Fgfr2-null mutants. On p. 723, Fen Wang's group report, from their studies of conditional Fgfr2 mutant embryos,that FGFR2 is required for prostate growth and morphogenesis and for certain aspects of this organ's androgen dependency. Branching morphogenesis is particularly affected in these mutants, and despite the continued ability of Fgfr2 conditional mutant prostates to secrete proteins in response to androgen, their ability to regulate tissue maintenance in an androgen-dependent manner is compromised. As advanced prostate tumours can often grow independently of androgen, further studies into the molecular mechanisms that define how FGFR2 regulates the prostate's maintenance and growth in an androgen-dependent manner could yield new therapeutic targets for the treatment of these aggressive cancers.