The aim of the present study was to: i) refine the location of the candidate gene(s) for risk and size of UL; ii) test whether FH is also mutated in UL but a presumably marked allelic heterogeneity at this locus, similar to that observed in HLRCC (Tomlinson et al. 2002, Bayley et al. 2008) precluded detection of associations; and iii) test for the presence of alternative susceptibility loci in the FH region that might associate with UL and would explain up to 40% of women with HLRCC-associated UL that do not carry mutations in FH (Tomlinson et al. 2002). This evidence concerns the gene FH and familial hyperaldosteronism.