In summary, because ILK is activated in response to IL-6 and other environmental signals,34, 45 the unique ability of ILK to regulate MUC1-C stability, in conjunction with STAT3-activated MUC1 gene expression,22 enables pancreatic cancer cells to interact with stress signals in the tumor microenvironment, such as IL-6 and hypoxia. This evidence concerns the gene MUC1 and pancreatic neoplasm.