Many bacterial pathogens replicate inside human cells by avoiding cell intrinsic innate immune pathways and subverting host cell metabolism. This subversion of host cell biology by intracellular pathogens more than often requires the transport of bacterial virulence effector proteins into the infected cell. Legionella pneumophila is an intracellular pathogen that replicates in human alveolar macrophages in a modified vacuole that resembles host endoplasmic reticulum. Biogenesis of the Legionella containing vacuole requires the concerted action of more than 300 bacterial effector proteins that extensively alter macrophage biology. We recently identified an effector protein from L. pneumophila that drives the degradation of a specific subset of mRNAs encoding glycolytic enzymes during infection of human macrophages. The effector protein bound directly to host mRNA and further investigation showed that L. pneumophila actively inhibited glycolysis but not mitochondrial respiration during infection. The consequences of this for the inflammatory response of infected macrophages is under investigation. In summary, the activities of effector proteins can provide new insight into the inflammatory, metabolic, cell death and cell intrinsic defense pathways that restrain pathogen replication and are important tools to understand the innate responses required for pathogen control.