These findings suggest that TLR/PI3K/AKT-activated EPRS1 phosphorylation at Ser999 directs the first line of anti-inflammatory immune defense against inflammatory signals, including bacterial infection, while IFNγ-mediated EPRS1 phosphorylation at Ser999 shapes translational fine tuning to protect cells from inflammation and injury in the presence of persistent inflammatory stimuli. This evidence concerns the gene AKT1 and bacterial infectious disease.