Francisella tularensis is a highly infective Gram-negative bacterium, that casues tularemia, which causes diseases in humans and mammals. It is able to survive and replicate within macrophages and protozoa cells, but its natural reservoir and the way of transmission are still mainly unknown. To maintain its life cycle, Francisella has to be able to modulate host cell death pathways. Previous research has shown that F. novicida is able to both postpone the cell death of human monocyte-derived macrophages and induce apoptosis of the infected cells. It has been shown that the iglC, which is part of Francisella pathogenicity island (FPI), plays a role in intracellular survival and cytopathogenic effect on the infected macrophages cells. There is no data about the induction of cell death by Francisella in amoebae cells. In this study, the role of apoptosis and the role of iglC gene on the cell death of Acanthamoeba castellanii was investigated. The amoeba cells were infected with F. novicida and the iglC mutant, and the cell death was measured after 2, 4, and 6 hours using flow cytometry. The results indicated that F. novicida blocks the induction of apoptosis in the early time point of infection. However, the iglC does not play a role in this process. Supressing the apoptosis enables for the bacterium to multiply for the longer period in this aquatic reservoir in the nature.