Salmonella Typhimurium is a bacterial pathogen with an intestinal tropism, causing foodborne diseases. To infect its hosts Salmonella employs a wide range of virulence factors that allow it to actively invade, survive and multiply in a vacuole or in the cytosol. The Salmonella Pathogenicity Island 1-encoded type III secretion system (T3SS1) was the first virulence factor described for its involvement in the invasion process and intracellular fate of Salmonella in the host cell. T3SS1 effectors coordinately mimic various host-cells protein functions, to hijack the cellular machinery allowing, Salmonella invasion and the initiation of the Salmonella containing vacuole (SCV) maturation. Since, two virulence factors Rck and PagN were shown to be involved in the invasion process. Recently, out of fifteen cell lines tested we identified five, in which the Salmonella Typhimurium invasion process is independent of the three known invasion factors. Here, we investigated the intracellular fate of Salmonella Typhimurium in the murine hepatic cell line AML12. We demonstrated that both wild-type Salmonella and T3SS1-invalidated Salmonella followed a common pathway beginning by the formation of a Salmonella containing vacuole (SCV) without classical recruitment of Rho- GTPases ending to Salmonella multiplication in SCV harboring Salmonella inducing filament. These results demonstrate that Salmonella invasion can be completely independent of the T3SS-1, and suggest that other bacterial players allow SCV early maturation. This model is of major interest for establishing the protein composition of an independent T3SS-1 SCV. A better knowledge of these vacuoles will allow the identification of new bacterial and host players necessary for the intracellular survival of Salmonella.