Background and Objective: Globally, Gastric Cancer (GC) is one of the leading causes of death associated with cancer. Over-expression of FOXM1 (forkhead box M1) has been observed in various cancers, implying that it plays a role in cancer progression. The study aims to examine the effect of Siomycin A on the AKT/FOXM1 signalling pathway, which can open new avenues in GC treatment. Materials and Methods: The cytotoxicity of Siomycin A was monitored on GES and SGC-7901 cell lines using the MTT assay. Effects on migratory ability and apoptosis were studied in the presence or absence of Siomycin A. Finally, the expression pattern of Bax, Bcl2, cleaved Caspase-3, FOXM1, AKT and pAKT was monitored to study the effect of Siomycin A. Results: FOXM1 was found to be highly over-expressed in GC cells. Siomycin A reduced the viability of gastric cancer cell line, SGC-7901, in a dose-dependent manner with minimal toxicity on normal gastric epithelial cells, GES. Furthermore, Siomycin A significantly induced apoptosis, altered the ratio of pro-and apoptotic markers and inhibited the migratory properties of SGC-7901 cells. Treatment of SGC-7901 cells with Siomycin A significantly downregulated AKT phosphorylation and FOXM1 expression. Conclusion: The results show Siomycin A prevented GC cell proliferation by downregulating the AKT/FOXM1signalling pathway. Furthermore, it is possible to infer from this study that Siomycin A may be used in the treatment of GC.