Objective: To study the expressions of two isoforms of Livin in tissues of lung cancer and their relations to histological types and chemotherapy, and to study their correlations to the expression of caspase-3 as well. Methods: Ex-pressions of Livin isoforms α, β and caspase-3 were detected by reverse transcription polymerase chain reaction (RT-PCR) assay in lung cancer tissues as well as in controls. Results: Livin isoforms α and β were expressed in 12 of 27, and 19 of 27 lung cancer tissues respectively, much more than those in lung para-cancerous [both were (0/6)] or benign disease lung tissues (0/12, 1/12; P < 0.01 and P < 0.01). Moreover, they were detected in 7/14, 9 /14 lung adenocarcinomas and 4/12, 9/12 squamocellular and large cell carcinomas, respectively, and both showed expressions in one small cell carcinoma. The levels of these two isoforms in lung cancer were significantly higher than those in controls by Gel imaging system (P < 0.05 and P < 0.05), the former was higher in adenocarcinoma than that in squamocellular carcinoma (P < 0.05), while the latter was the same in both (P > 0.05). Meanwhile, the levels of caspase-3 in lung cancer were significantly lower than those in controls, and it was suggested to be negatively associated with either each of two isoforms or their sum (P < 0.05, P < 0.01 and P < 0.01). Two isoforms of Livin expression seemed to increase after chemotherapy but not related to clinical stages (P > 0.05). Conclusion: Two isoforms of Livin are differently expressed in different histological types of lung cancer and may contribute to corresponding cancerous development; the levels of Livin are negatively associated with those of caspase-3, this may be due to the fact that Livin could resist against apoptosis; high expression of Livin seems to be related to chemotherapy but not clinical stages. Objective: To study the expressions of two isoforms of Livin in tissues of lung cancer and their relations to histological types and chemotherapy, and to study their correlations to the expression of caspase-3 as well. Methods: Ex-pressions of Livin isoforms α, β and caspase-3 were detected by reverse transcription polymerase chain reaction (RT-PCR) assay in lung cancer tissues as well as in controls. Results: Livin isoforms α and β were expressed in 12 of 27, and 19 of 27 lung cancer tissues respectively, much more than those in lung para-cancerous [both were (0/6)] or benign disease lung tissues (0/12, 1/12; P <0.01 and P <0.01) / 14, 9/14 lung adenocarcinomas and 4/12, 9/12 squamocellular and large cell carcinomas, respectively, and both were expression in one small cell carcinoma. The levels of these two isoforms in lung cancer were significantly higher than those in controls by Gel imaging system (P <0.05 and P <0.05), the former was hi gher in adenocarcinoma than that in squamocellular carcinoma (P <0.05), while the latter was the same in both (P> 0.05). Meanwhile, the levels of caspase-3 in lung cancer were significantly lower than those in controls, and it was suggested to be negatively associated with either each of two isoforms or their sum (P <0.05, P <0.01 and P <0.01). Conclusion: Two isoforms of Livin are differently expressed in different histological types of lung cancer and may contribute to corresponding cancerous development; the levels of Livin are negatively associated with those of caspase-3, this may be due to the fact that Livin could resist against apoptosis; high expression of Livin seems to be related to chemotherapy but not clinical stages.