also used pancreas cancer xenograft in CDH11 deficient and wild-type mice models to demonstrate using IMC that the inhibition of CDH11, expressed by cancer-associated fibroblasts, caused a reduction in tumor growth, increased the tumor response to gemcitabine and was implicated in immunosuppression and extracellular matrix deposits consisting the highly fibrotic stroma of pancreatic ductal adenocarcinoma (57). Here, CDH11 is linked to pancreatic ductal adenocarcinoma.