The study demonstrated that S100A10 was upregulated in PDAC tumour tissue and high-grade PanINs, including PanIN-1B, PanIN-2 and PanIN-3, relative to normal epithelium, pancreatitis and low-grade PanINs, such as PanIN-1A, which suggests that S100A10 plays a key role in the progression of the disease into an invasive phenotype. This evidence concerns the gene S100A10 and pancreatitis.