Zeng et al.7, for instance, found that S100A11 was overexpressed in pancreatic ductal adenocarcinoma (PDAC) and had a strong link with a poor prognosis and disease progression in patients, which mechanistically demonstrated that S100A11 could induce malignant biological behaviors, including proliferation and migration of PDAC cells, by activating the pentose phosphate pathway. This evidence concerns the gene S100A11 and pancreatic ductal adenocarcinoma.