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Targeted deletion of mouse activating transcription factor 3 (ATF3) gene increased lipopolysaccharide (LPS)-driven airway epithelia production of CXCL1 without increasing airway neutrophilia after LPS challenge. On the other hand, recruitment of ATF3^−/− neutrophils to inflamed WT lungs was impaired. In vitro, ATF3^−/− neutrophils exhibited a profound chemotaxis defect and increased focal complex area, and excessive F-actin polymerization. ATF3-mediated expression of Tiam2, a critical regulator of focal adhesion disassembly, was required for neutrophil chemotaxis and focal complex assembly. The image shows the excessive formation of actin polymerization and focal complex area in ATF3^−/− neutrophils, which were stained with rhodamine-phalloidin (red) for F-actin and rabbit anti-vinculin (green) for focal complexes. See the article by Boespflug et al on page 2084.