The RAS pathway, known as the Ras/Raf/MAPK pathway, is a crucial signal transduction cascade that regulates essential cellular processes, including growth, differentiation, and survival. Central to this pathway is the RAS protein, a small GTPase that acts as a molecular switch, alternating between inactive GDP-bound and active GTP-bound states. Activation of RAS is initiated by extracellular signals, primarily through the binding of ligands to receptor tyrosine kinases (RTKs), which subsequently activate guanine nucleotide exchange factors (GEFs) and the conversion of GDP to GTP. Notably, mutations in the RAS gene, especially the KRAS G12C mutation, are implicated in various cancers, particularly non-small cell lung cancer (NSCLC) and colorectal cancer (CRC), where they lead to uncontrolled cell proliferation and tumorigenesis. This study examines the intricate roles of KRAS, including its domains, isoforms, and mutation profiles, and discusses emerging therapeutic approaches targeting KRAS mutations, such as specific inhibitors like Adagrasib. A comprehensive understanding of the RAS pathways complexities and its oncogenic potential is essential for advancing targeted therapies and enhancing cancer treatment outcomes.