【Abstract】 Objective To investigate the role of inhibitor of apoptosis protein, livin, in response to sorafenib of 786- 0 cell lines and molecular mechanism. Methods Immunohistochemistry was performed to evaluate the expression of livin in normal kidney tissues and RCC tissues. Livin was overexpressed in 786-0 cell lines by lentivirus containing livin-over- expressed plasmid. MTT was performed to detect the response of 786-0 NC and 786-0 livin-overexpressed cell lines to sorafenib. Western blot was used to elucidate the mechanism through which livin conferred 786-0 cell lines resistant to sorafenib. Result Compared with normal kidney tissues, livin was upregulated in RCC tissues. The expression difference of livin between normal kidney tissues and RCC was statistically significance (PVO. 0001). Livin-overexpressed 786-0 showed resistance to different concentration of sorafenib (3 uM, 6 uM, 9 uM) after treated for 48 hours in comparison to NC. Cleaved caspase 3 was elevated in 786-0 NC that was treated with sorafenib (9 uM) for 48 hours. Livin could rescue the expression of cleaved caspase 3 in 786-0 that was treated with sorafenib (9 uM) for 48 hours. Conclusion Livin could modulate the response of RCC to sorafenib through regulating the expression of cleaved caspase 3.