As 14-3-3β co-localizes with the chlamydial protein IncG on the surface of the inclusion [32], these results suggest that this IncG-14-3-3β interaction allows the inclusion to sequester BAD away from mitochondria, where it could stimulate release of cytochrome c. Simultaneous activation of the PI3K pathway during infection maintains BAD in its phosphorylated state (Figure 9). Here, BAD is linked to infection.