Objective: To explore the correlation between nephrosis-related growth arrest specific 6(Gas6) and nephrotic syndrome and apoptosis. The effect of AP-2 transcription factor a(TFAP2A) on Gas6 was investigated. Methods:The cell model of adriamycinnephropathy(AN) was constructed to detect the expression of Gas6, and MPC5 cells were stimulated with Gas6 protein to measure the expression of nephropathy related indicators. HEK-293T cells were intervened with Gas6 protein to measure apoptosis rate or the expression of apoptosis-related indicators. The luciferase gene reporter recombinant plasmid of Gas6 promoter was constructed to measure the activity of Gas6 promoter in HEK-293T cells. And the potential transcriptional binding sites were predicted and verified. The effects of knockdown or overexpression of TFAP2A on Gas6 gene expression were measured at the promoter, mRNA, and protein levels. Results: Gas6 was highly expressed in AN cell model, and excessive Gas6 may induce the nephropathy-related indicators in MPC5 cells the same trend as that of AN cell model. Apoptosis was significantly reduced in the Gas6 protein group compared to control in HEK-293T cells.The active luciferase reporter plasmid of human Gas6 promoter fragment was successfully constructed, and the binding sites of TFAP2A were included. TFAP2A positively regulates Gas6 at the promoter, mRNA, and protein levels. Conclusion: Gas6 promotes the development of nephrotic syndrome. Gas6 is antiapoptotic in HEK-293T cells. TFAP2A positively promotes the expression of human nephrosis-related gene Gas6.