Furthermore, we showed that in KRAS-mutated cancer cells, RTK-SOS2-WT RAS signaling was necessary to provide adequate PI3K/AKT signaling for cells to survive in anchorage-independent growth conditions (protection from anoikis) [81], but HRAS- and NRAS-mutated cancer cells could survive in anchorage-independent conditions without RTK-SOS2 supplemented PI3K signaling [82]. This evidence concerns the gene NRAS and cancer.