Notably, this approach allowed us to narrow down the cell types in which ORMDL3 potentially influences disease outcomes, and, therefore, perform detailed functional studies in a relevant cell type (primary human CD4+ T cells) and show that ORMDL3 negatively regulates the transcription of IL2. Given the pleotropic role of IL-2 in modulating the differentiation and function of TH cell subsets, it is likely that this effect on IL-2 production could be pivotal for driving genetic risk for asthma and autoimmunity. This evidence concerns the gene CD4 and Autoimmunity.