Increased Ral activity has also been shown in KRAS-4B G12V-mutant pancreatic cancer, due to altered binding kinetics and a more dynamic interaction between KRAS-4B G12V and the RalGEF Rgl2, compared to the KRAS WT interaction with Rgl2 (Tariq et al., 2024). Here, KRAS is linked to pancreatic neoplasm.