The untreated mice that developed ALI/ARDS presented pleural effusion, hemorrhaging and intense inflammatory infiltration on the day of death (Fig 4C); however, AMD3100 treated-mice showed only minimal thickening of the alveolar septa on the day of death, indicating that blocking the action of CXCR4 with AMD3100 was effective in reducing the pathological responses associated with the decrease in neutrophils in the lungs of AMD3100-treated mice, on the 7th dpi (Fig 4D). The gene discussed is CXCR4; the disease is Pleural effusion.