Introduction: Intestinal atresia occurs in 1:1000 live births and represents one of the most common forms of neonatal intestinal obstruction leading to short bowel syndrome. It is known that the FGF10/Fgfr2b signaling pathway plays a critical role in the regulation of proliferation and apoptosis in multiple organ systems including the developing lungs, limbs, and gastrointestinal tract (GIT). Furthermore, we have shown that loss of either GIT mesenchymal FGF10 or epithelial Fgfr2b, results in a failure of proliferation and subsequently, in intestinal atresia. The functional mechanism of mesenchymal FGF10 signaling through its epithelial receptor Fgfr2b remains to be elucidated. Furthermore, regulation of Fgfr2b has not been fully evaluated.mShisa is an endoplasmic reticulum retention modulator protein that is known to bind with receptors in the FGFr family. It has been suggested that mesenchymal expression of mShisa is up-regulated during development. Our preliminary data suggests its abundance in the epithelium and up-regulation in all stages of GIT development. We hypothesize that mShisa may serve a regulatory role in the FGF10/Fgfr2b signaling pathway during GIT embryogenesis.Methods: We evaluated the expression patterns of mShisa using an RNA probe, produced and used to perform whole mount in situ hybridization (wmISH) on the intestine of E13-E15 mice. The expression pattern was also evaluated with RT-PCR. In order to validate the correlation of mShisa with Fgfr2b, we also performed wmISH on E13-E15 mice GIT using an Fgfr2b RNA probe.Results: wmISH data demonstrates abundant GIT epithelial expression of mShisa during development. We also confirm its up-regulation at all stages of GIT development using RT-PCR. In addition, we demonstrate that FGFr2b expression pattern is co-distributed with mShisa in the developing GIT.Conclusion: Our data shows the abundant epithelial expression of mShisa and its up-regulation at all stages of GIT development. Furthermore, mShisa is known to bind Fgf receptors in the endoplasmic reticulum and Golgi complex where Fgf receptors are known to undergo post-transcriptional modification. Our findings suggest a potential regulatory role of mShisa on the FGF10/Fgfr2b signaling pathway.