Ras mutations contribute to cancer by causing the encoded proteins to become constitutively active, meaning they are always "on." This continuous activation leads to persistent signaling through downstream pathways such as the MAPK/ERK and PI3K/AKT pathways, promoting cell growth, survival, and proliferation. Consequently, cells with Ras mutations can evade normal regulatory mechanisms that control cell division and apoptosis, leading to tumorigenesis.
