They found that this gene variant induced a significant alteration in the surface structure of Maspin protein and wild-type Pro176 Maspin efficiently induced apoptosis by activating caspase-3 and repressed colony formation of NCI-H157 cells, human lung cancer cell line and decreased tumorigenesis in lung cancer cells in nude mice, but the ability of Ser176 Maspin to stimulate caspase-3 activity was significantly decreased and it was associated with decreased in vitro apoptosis and increased in vivo tumorigenesis [16]. This evidence concerns the gene CASP3 and lung cancer.