IL‐33 signals through ST2, which is expressed either as a full‐length signaling receptor or a truncated soluble receptor that can suppress IL‐33 activity. Previous data suggest that soluble ST2 mRNA in fibroblasts is coupled to a serum‐inducible proximal promoter, while full‐length ST2 expression in immune cells is directed from a distal promoter. In order to better understand the function of the alternative promoters and how they ultimately affect the regulation of IL‐33, we generated a mouse in which the ST2 proximal promoter is deleted. Promoter deletion had no impact on ST2 expression in mast cells or their ability to respond to IL‐33. In contrast, it resulted in a complete loss of both soluble and full‐length ST2 mRNA in fibroblasts, which corresponded with both an inability to secrete soluble ST2 and a defect in IL‐33 responsiveness. Importantly, in spite of the fibroblast defect, soluble ST2 concentrations were not reduced in the serum of naïve or allergen‐exposed knockout mice. In summary, we found that ST2 promoter usage is largely cell‐type dependent but does not dictate splicing. Moreover, the proximal promoter is not a major driver of circulating soluble ST2 under the conditions tested.