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YKL-40, which is a chitinase-like protein, is produced by various inflammatory cells and may have an important role in asthma development and disease deterioration. The associations between CHI3L1 and asthma have been replicated in other populations, but further studies on asthma and asthma-related phenotypes are warranted [24]. As of January 2012, the results of 21 GWASs of asthma or asthma-related traits had been published and markers in 36 genes had been identified with a commonly used cut-off of P?��?10?6 for association (Table?1) [46]. To further explore the biology of the genes identified in GWASs, we performed gene ontology (GO) enrichment analysis using the Database for Annotation, Visualization and Integrated Discovery (DAVID) [47, http://www.selleckchem.com/products/z-vad-fmk.html 48]. In terms of bio-ontologic enrichment, the genes shown to be associated with asthma in GWASs were enriched (P? http://www.selleck.cn/products/BIBW2992.html (IL) receptors, as well as the IL33 loci confer involvement of the IL gene family and their receptors in asthma. IL33 with its receptor IL1RL1 belongs to the IL1 family of cytokines that are known to be expressed on epithelial cells and are involved in the host response to certain environmental and infectious stimuli [49]. Severe asthma has been particularly studied in two GWASs, both of which indicated the importance of Th2-like genes in the locus on chromosome 5q containing RAD50 and IL13 [50], and TSLP on the same chromosome [36]. In addition, association with HLA-DQB1 was observed [50]. Using emergency department visits or hospitalizations as the definition of a severe asthma exacerbation in the CAMP study, a combination of 160�C320 SNPs were http://www.selleckchem.com/products/ly2157299.html found to predict exacerbation with an area under the curve (AUC) of 0.66 [51]. For a complex trait such as severe asthma, prediction has proven to be very challenging, and the AUC in this study shows that genetic analyses can improve our diagnostic tools, although much work remains before clinical testing can become a reality. Amongst the top 160 SNPs identified in the CAMP study, one (rs10496476) is located within DPP10, which was identified as an asthma-susceptibility gene by positional cloning [14].