SPTLC2 and inflammatory bowel disease: Therefore, in our present study, we created intestine-specific inducible Sptlc2 KO mice and found that a deficiency of sphingolipid de novo biosynthesis in the intestine promoted cell apoptosis, damaged intestine integrity, and increased intestinal permeability (Fig. 5f); moreover, patients with an inflammatory bowel disease were found to have a significantly lower level of colon SPTLC2 mRNA and of SPTLC2 staining intensity (Fig. 6a–d).