For instance, in a spontaneous pancreatic cancer transgenic model (KPC mice), quantitative immunohistochemical analyses revealed that although GOT2 protein expression is markedly downregulated in tumor epithelial cells, cancer-associated fibroblasts (CAFs) retain high levels of GOT2 expression, suggesting a compensatory role in stromal remodeling (12). Here, GOT2 is linked to pancreatic neoplasm.