Abstract
ADAM33 has been described to be the first positional cloned asthma gene. Consecutive association studies have found inconsistent results. At present no functional relevant variation is being known. Aim of the study was to test if genes in close physical distance could also be responsible for the observed linkage signal. We downloaded three public single-nucleotide polymorphism (SNP) data sets and tested if linkage disequilibrium extends beyond ADAM33. Linkage disequilibrium extends upstream to a region including GDNF family receptor alpha (GFRA4), attractin (ATRN) and downstream to sialoadhesin (SN) with a peak recombinatory rate at ADAM33 exon S to V. Resequencing of the ADAM33 region including GFRA4, ATRN and SN is expedient.