As the driver gene of lung cancer, Kirsten rat sarcoma viral oncogene (KRAS) mutation often occurs in lung adenocarcinoma resistant to treatment with epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs), which has attracted attention due to its poor prognosis and lack of targeted drugs. Recent studies have found that KRAS mutation can promote tumor progression and affect treatment and prognosis by affecting the expressions of signal transducer and activator of transcription 3 (STAT3), G-protein-coupled receptor (GPCR) and programmed death receptor-ligand 1 (PD-L1), mammalian target of rapamycin (mTOR) signaling pathway activation and co-mutation of multiple genes. A phase Ⅰ clinical trial shows that AMG 510, a novel small molecule KRAS G12C inhibitor, is hopeful in treatment. Summarizing the pathogenesis, prognostic factors, targeted therapy and immunotherapy of KRAS mutation in lung adenocarcinoma is helpful to improve the understanding of KRAS mutation and can provide ideas and basis for subsequent studies.