This work and the earlier ACH testes biopsy data (14) provide a rationale for suggesting it is likely that this process is driven by biological mechanisms similar to those already suggested for the two most common Apert syndrome mutations in the receptor tyrosine kinase FGFR2 (19–22,24) and the MEN2B mutation in the receptor tyrosine kinase RET (19). Here, FGFR2 is linked to Apert syndrome.