To test this hypothesis, Yang et al. overexpressed CXCR4/GFP or GFP in MSCs using a lentiviral vector and subsequently investigated them in a rat model of ALI injured by LPS, demonstrating that CXCR4-MSCs showed improved homing and colonization of injured lung tissue compared with the control GFP-MSCs, which resulted in a decrease in the levels of pro-inflammatory cytokines and neutrophil numbers in bronchoalveolar lavage fluid (BALF) [53]. This evidence concerns the gene CXCR4 and acute respiratory distress syndrome.