The intracellular pathogen Legionella pneumophila exploits host cell vesicular transport by manipulating the activity of the small GTPase Rab1. Bacterial proteins, so called effectors, that are delivered into the infected cell play a key role in this process. Here, we summarize recent developments in our quest to understand the molecular function of these effectors, and describe how L. pneumophila employs post-translational modification in a reversible manner to manipulate the activity of Rab1 on its vacuole.