RAS oncogenes are essential components of signaling pathways originating from cell surface receptors. Mutations in RAS genes are frequently found in various cancers and are known to drive tumorigenesis by activating complex molecular circuits. The discovery of RAS's transforming properties in the late 1970s led to the identification of other cancer-related genes and the concept that cancer progression involves the accumulation of genetic changes that enable cancer cells to evade homeostatic barriers. These changes, known as the hallmarks of cancer, include self-sufficiency in growth signals, insensitivity to growth-inhibitory signals, evasion of programmed cell death, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. Recent additions to this list include metabolic fitness and genomic plasticity. Oncogenic RAS activation is primarily due to mutations that impair GTP hydrolysis, leading to persistent activation of downstream signaling pathways. Different RAS mutations may lead to similar pathophysiological outcomes, but specific mutations like KRASG12V are associated with worse prognoses. Studies show that different RAS isoforms (HRAS, NRAS, KRAS) are associated with various cancers, and their functional roles are influenced by tissue-specific regulatory elements. RAS oncogenes promote cell proliferation by disrupting mechanisms that regulate cell cycle progression and by enhancing the expression of growth factors and receptors. They also contribute to the evasion of apoptosis by downregulating pro-apoptotic mediators and upregulating anti-apoptotic molecules. RAS-driven metabolic reprogramming involves increased glucose uptake and aerobic glycolysis, which supports cancer cell growth. RAS also promotes angiogenesis by inducing the production of vascular endothelial growth factor (VEGF) and other pro-angiogenic factors, which facilitate tumor growth. RAS oncogenes can also evade immune surveillance by reducing the expression of MHC molecules and recruiting immunosuppressive cells. Metastasis is another key aspect of cancer progression, where RAS contributes by promoting cell invasion, migration, and the ability to spread to distant organs. RAS signaling pathways, such as RAS-MAPK, RAS-PI3K, and RAS-RHO, are involved in multiple steps of metastasis, including cell adhesion, motility, and intravasation. Despite significant progress in understanding RAS oncogenes, many aspects of their role in cancer remain unclear. New experimental tools are enabling deeper insights into RAS-driven cancer mechanisms, offering opportunities for developing targeted therapies. The context-dependent nature of RAS function highlights the complexity of its role in cancer, and further research is needed to fully understand its contributions to tumorigenesis and metastasis.RAS oncogenes are essential components of signaling pathways originating from cell surface receptors. Mutations in RAS genes are frequently found in various cancers and are known to drive tumorigenesis by activating complex molecular circuits. The discovery of RAS's transforming properties in the late 1970s led to the identification of other cancer-related genes and the concept that cancer progression involves the accumulation of genetic changes that enable cancer cells to evade homeostatic barriers. These changes, known as the hallmarks of cancer, include self-sufficiency in growth signals, insensitivity to growth-inhibitory signals, evasion of programmed cell death, limitless replicative potential, sustained angiogenesis, and tissue invasion and metastasis. Recent additions to this list include metabolic fitness and genomic plasticity. Oncogenic RAS activation is primarily due to mutations that impair GTP hydrolysis, leading to persistent activation of downstream signaling pathways. Different RAS mutations may lead to similar pathophysiological outcomes, but specific mutations like KRASG12V are associated with worse prognoses. Studies show that different RAS isoforms (HRAS, NRAS, KRAS) are associated with various cancers, and their functional roles are influenced by tissue-specific regulatory elements. RAS oncogenes promote cell proliferation by disrupting mechanisms that regulate cell cycle progression and by enhancing the expression of growth factors and receptors. They also contribute to the evasion of apoptosis by downregulating pro-apoptotic mediators and upregulating anti-apoptotic molecules. RAS-driven metabolic reprogramming involves increased glucose uptake and aerobic glycolysis, which supports cancer cell growth. RAS also promotes angiogenesis by inducing the production of vascular endothelial growth factor (VEGF) and other pro-angiogenic factors, which facilitate tumor growth. RAS oncogenes can also evade immune surveillance by reducing the expression of MHC molecules and recruiting immunosuppressive cells. Metastasis is another key aspect of cancer progression, where RAS contributes by promoting cell invasion, migration, and the ability to spread to distant organs. RAS signaling pathways, such as RAS-MAPK, RAS-PI3K, and RAS-RHO, are involved in multiple steps of metastasis, including cell adhesion, motility, and intravasation. Despite significant progress in understanding RAS oncogenes, many aspects of their role in cancer remain unclear. New experimental tools are enabling deeper insights into RAS-driven cancer mechanisms, offering opportunities for developing targeted therapies. The context-dependent nature of RAS function highlights the complexity of its role in cancer, and further research is needed to fully understand its contributions to tumorigenesis and metastasis.