KRAS and cancer: Additionally, dietary n-3 PUFAs in genetic KRasG12D mutant mice in vivo and in vitro show that n-3 PUFAs physically merged into a phospholipids layer of the cellular membrane to reduce the lateral segmentation of cholesterol-dependent and independent nanoclusters and accordingly inhibit the interaction of oncogenic KRAS signaling effectors [27], implying that the disruption of membrane nanoclustering might overcome oncogenic KRAS-induced tumorigenesis and cancer progression.