IgE dysregulation is a major pathogenic feature of atopic dermatitis and other IgE-mediated allergic diseases such as asthma and rhinitis. Allergen complexed to IgE binds to the high affinity receptor for IgE (FcεRI) on the surface of epidermal Langerhans cells, mast cells and basophils, triggering the release of inflammatory mediators. The β subunit of FcεRI has been localized to human chromosome 11q12–13, and variants within this gene have been shown to associate with asthma and measures of atopy. We have tested several polymorphisms within FcεRI-β for association to atopic dermatitis in a panel of 60 families (panel A), recruited through a proband with atopic dermatitis. The findings were tested in a second panel of families (panel B). Significant sharing of maternal alleles was seen for atopic dermatitis and allele 2 of RsaI intron 2 (RsaI_in2*2) (= 0.0022) and allele 1 of RsaI exon 7 (RsaI_ex7*1) (= 0.0036) FcεRI-β gene polymorphisms. These findings were replicated in Panel B, confirming the association of FcεRI-βRsaI polymorphisms with atopic dermatitis. The combined significance of the association of atopic dermatitis to RsaI polymorphisms was = 0.0002 (RsaI_in2*2) and = 0.00034 (RsaI_ex7*1). The polymorphisms also showed association with asthma: = 0.0068 (RsaI_in2*2) and = 0.018 (RsaI_ex7*1). Polymorphisms within the FcεRI-β gene are strongly associated with atopic dermatitis.