Some patients believe that lung cancer is hereditary, while others believe that lung cancer is not hereditary. First-degree relatives of lung cancer patients have a 2 to 3 times increased risk of developing lung cancer or other tumors. Lung cancer cells have many genetic damages, including activation of proto-oncogenes, inactivation of oncogenes, activation of the self-feedback secretion loop and inhibition of apoptosis, resulting in uncontrolled cell growth. In fact, lung cancer cells may have multiple (possibly ≥10) genetic abnormalities. The main oncogenes that are closely associated with lung cancer are the ras and myc gene families, c-erbB-2, Bcl-2, c-fos, and c-jun genes. Related oncogenes include p53, Rb, CDKN2, FHIT genes, etc. Molecular alterations associated with lung carcinogenesis and progression also include abnormalities in mismatch repair genes such as hMSH2 and hPMS1, and expression of telomerase. These genetic alterations arise multistep and randomly over a long period of time. The main oncogenes that are closely associated with lung cancer are the ras and myc gene families, c-erbB-2, Bcl-2, c-fos, and c-jun genes. The related oncogenes include p53, Rb, CDKN2, FHIT genes, etc. Molecular alterations associated with lung cancer development and progression also include abnormalities in mismatch repair genes such as hMSH2 and hPMS1, and expression of telomerase. It can be seen that lung cancer is genetically related, but the development of lung cancer also requires the influence of the external environment, which results in mutations in genes that lead to cancer.