Lung cancer remains the leading cause of cancer-related deaths in men and women worldwide, and 85% of these patients have non-small cell lung cancer. In recent years, the clinical use of targeted drug therapy and immune checkpoint inhibitors has dramatically changed the treatment landscape for advanced NSCLC. The mechanism and the value of targeted therapies have been a hot topic of research, as is one of the earliest discovered and most frequently mutated oncogenes, which is activated by binding to GTP and triggers a series of cascade reactions in cell proliferation and mitosis. The protein acts as a molecular switch and is activated by binding to GTP, triggering a series of cascade responses in cell proliferation and mitosis. Clinically, patients with mutated NSCLC have poor response to systemic medical therapy and poor prognosis. Since the first report of gene in 1982, research on targeted therapeutics has been slow, and previous studies such as farnesyltransferase inhibitors and downstream protein inhibitors of signaling pathway have not achieved the expected results, making long defined as a "non-druggable target". The deeper understanding of the crystal structure of has led to the discovery of potential therapeutic sites for and the development of several drugs directly targeting especially G12C inhibitors such as AMG510 (sotorasib) and MRTX849 (adagrasib), which have shown encouraging results in clinical trials. In recent years, studies on the therapeutic efficacy of immune checkpoint inhibitors for -mutated NSCLC have made some progress. In this review, we systematically introduce the basic understanding of gene and clinical characteristics of mutated NSCLC patients, summarize the medical treatments for mutated NSCLC, including chemotherapy, anti-vascular drug therapy and tumor immunotherapy, and focus on the review and outlook of the research progress of targeted therapy.