KRAS mutations occur in approximately 95% of pancreatic cancers. Most of these mutations promote aggressive tumor growth and resistance to treatment. The KRAS G12R mutation is present in about 15% of cases, and patients with it have better outcomes, including earlier diagnosis, better response to treatment, and longer survival. In mouse models, the G12R mutation did not cause pancreatic cancer to develop even after a year, unlike common KRAS mutations that lead to aggressive metastatic disease. This mutation in human pancreatic cancer cells does not activate the PI3K pathway, although it activates ERK, which differs from mouse models. Tumors with KRAS G12R have weaker cells with slower movement, a lower ability to remodel surrounding tissue, less collagen, which makes them more permeable, and a lower ability to migrate, which limits metastasis.