Background: Cancer is currently one of the leading causes of death in the Americas, with incidence projected to increase in the coming decades. Metastasis, responsible for the majority of cancer-related deaths, is associated with epithelial-mesenchymal transition (EMT), a process regulated by complex gene networks and signaling pathways, such as nuclear factor kappa B (NF-κB). We investigated this process in Drosophila melanogaster, a model organism with high conservation of genes and signaling mechanisms, including homology between Dorsal (Drosophila) and NF-κB (mammals). Our study focuses on the target gene snail, whose abrupt expression pattern remains unexplained in the literature. Aim: To determine whether the abrupt expression pattern of snail can be explained by bistability in its regulatory network involving Dorsal and Twist, potentially enhanced by autoactivation mechanisms. Methodology: We developed a mathematical model based on biochemical reactions that describes the regulatory interactions of snail. Analytical investigations focused on identifying conditions for multiple steady states through zero eigenvalue analysis. A genetic algorithm was implemented to calibrate the model using experimental data. Results: Three potential autoactivation sites were identified in the snail promoter region. The model reproduced the bistable behavior and generated clear expression profiles, consistent with experimental observations. Knockout embryos showed smoother snail expression patterns, supporting the hypothesis that bistability contributes to boundary formation. Conclusion: Bistability in the snail regulatory network provides a plausible mechanism for the formation of its abrupt expression domain in Drosophila. These findings may reflect conserved regulatory strategies relevant to EMT and metastatic progression in humans.