In addition, SJP exhibited a stronger myeloid‐ and inflammation‐related DEG signature; JPS polyps exhibited more fibroblast‐expressed DEGs, which were involved in myofiber formation; and PJS polyps had distinctive transcriptional changes in epithelial cells, reflecting upregulated nutrient absorption and a downregulated response to TNF‐α as well as decreased p53 activity. The gene discussed is TP53; the disease is juvenile polyposis syndrome.