These data are in agreement with results showing that the Kallmann syndrome is caused by diminished signaling via the FGFR1 since, in contrast to the Craniosynostosis and chondrodysplasia syndromes [39] caused by point mutations resulting in excessive uncontrolled signaling, in Kallmann syndrome, the causal FGFR1 alterations are loss of function mutations [40]. This evidence concerns the gene FGFR1 and Kallmann syndrome.