Rationale: Microarray data from mouse studies has identified a number of genes to be differentially expressed in allergen-sensitized mice lungs. Taking leads from these datasets, we attempted to identify novel genes associated with atopic asthma in humans. Methods: We performed family based genetic association analysis on selected markers within or in proximity of 21 human homologs of genes short-listed from ovalbumin sensitized mice studies in GEO database of NCBI. Family-based and case-control studies were undertaken for fine mapping and functional variation analysis of Inositol polyphosphate 4 phosphatase type I (INPP4A). Western blot analysis was performed to analyze INPP4A protein stability from human platelets. Results: Our genetic association studies of 21 human genes in 171 trios led to the identification of a bi-allelic repeat (rs3217304) in INPP4A, associated with atopic asthma (P= 0.009). Further studies using additional three single nucleotide polymorphisms (SNPs), +92031A/T, +92344C/T, and +131237C/T and two microsatellite markers, D2S2311 and D2S2187, revealed significant genetic associations with loci +92031A/T (p=0.0012) and +92344C/T (p=0.004). A non-synonymous SNP +110832A/G^Thr/Ala present within a PEST sequence, in proximity of these two loci, showed a significant association with atopic asthma (p=0.0006). The association results were also replicated in an independent cohort of 288 patients and 293 controls (p=0.004). PEST score and western blot analyses indicated a functional role of this SNP in regulating INPP4A protein stability. Conclusions: In our study, INPP4A was identified as a novel asthma candidate gene, whereby the +110832A/G^Thr/Ala variant affected its stability and was significantly associated with asthma.