This study is to investigate the effect of (2-methyl-n-butyl) shikonin (MBS) on inducing apoptosis of human gastric cancer cell line SGC-7901 and the role of ERK1/2 signal pathway in the apoptosis.  MTT assay was used to detect SGC-7901 cell proliferation.  DNA condensation was measured by DAPI stain.  Cell apoptosis was analyzed by flow cytometry.  Mitochondrial membrane potential (MMP) was analyzed by JC-1 staining.  The protein expressions of Bcl-2, Bax, Survivin, cleaved caspase-9, cleaved caspase-3, cleaved PARP, p-ERK1/2, ERK1/2, p-JNK, JNK, p-p38 and p38 were detected by Western blotting.  The results showed that MBS reduced the cell viability of SGC-7901 cells in a dose- and time-dependent manner.  The IC₅₀ at 24 h and 48 h for SGC-7901 cells was 10.113 and 4.196 μmol·L⁻¹, respectively.  After being treated with MBS, the typical nuclear condensation was observed in SGC-7901 cells by DAPI stain.  Apoptosis in SGC-7901 cells was induced by MBS in a dose dependent manner.  The protein expression of Bcl-2 was down-regulated, while the protein expressions of cleaved caspase-9, cleaved caspase-3, cleaved PARP, p-ERK1/2 and p-JNK were up-regulated after MBS treatment.  U0126, a specific MAP kinase (MEK1/2) inhibitor, blocked the ERK1/2 activation by MBS.  MMP was decreased by MBS treatment.  It can be concluded that MBS could inhibit SGC-7901 cell proliferation and induce apoptosis.  Mitochondrial apoptosis pathway, ERK1/2 signal pathway and JNK signal pathway might be involved in this process.