RAS proteins are essential components of signaling pathways that originate from cell surface receptors. Oncogenic activation of these proteins, often due to missense mutations, is frequently observed in various types of cancer. This review discusses how RAS oncogenes exploit their extensive signaling capabilities to influence multiple cellular processes that drive tumorigenesis. The oncogenic activation of RAS proteins involves mutations that impair their GTPase activity, leading to their persistent activation and the activation of downstream effector pathways. The functional diversity of different RAS isoforms and their contributions to cancer aetiology remain areas of ongoing research. RAS oncogenes promote proliferation by enhancing the transcriptional upregulation of growth factors and altering the expression of growth factor receptors. They also suppress apoptosis by interfering with anti-apoptotic signaling pathways and promoting cell cycle progression. RAS oncogenes impact metabolism by upregulating hypoxia-inducible factor 1α (HIF1α), which stimulates glycolysis and glucose transport. Additionally, RAS oncogenes remodel the microenvironment by inducing angiogenesis and altering the extracellular matrix. They also evade the immune response by reducing the surface expression of major histocompatibility complexes and modulating immune cell function. Finally, RAS oncogenes contribute to metastasis by altering cell adhesion and motility, as well as protecting tumor cells from anoikis. The context-dependent nature of RAS oncogenic potential and the complex signaling networks involved highlight the challenges and opportunities in understanding and targeting RAS-driven cancers.RAS proteins are essential components of signaling pathways that originate from cell surface receptors. Oncogenic activation of these proteins, often due to missense mutations, is frequently observed in various types of cancer. This review discusses how RAS oncogenes exploit their extensive signaling capabilities to influence multiple cellular processes that drive tumorigenesis. The oncogenic activation of RAS proteins involves mutations that impair their GTPase activity, leading to their persistent activation and the activation of downstream effector pathways. The functional diversity of different RAS isoforms and their contributions to cancer aetiology remain areas of ongoing research. RAS oncogenes promote proliferation by enhancing the transcriptional upregulation of growth factors and altering the expression of growth factor receptors. They also suppress apoptosis by interfering with anti-apoptotic signaling pathways and promoting cell cycle progression. RAS oncogenes impact metabolism by upregulating hypoxia-inducible factor 1α (HIF1α), which stimulates glycolysis and glucose transport. Additionally, RAS oncogenes remodel the microenvironment by inducing angiogenesis and altering the extracellular matrix. They also evade the immune response by reducing the surface expression of major histocompatibility complexes and modulating immune cell function. Finally, RAS oncogenes contribute to metastasis by altering cell adhesion and motility, as well as protecting tumor cells from anoikis. The context-dependent nature of RAS oncogenic potential and the complex signaling networks involved highlight the challenges and opportunities in understanding and targeting RAS-driven cancers.