Deleting Rac1 in the mouse is embryonic lethal, but drug‐inducible conditional Rac1‐deficiency is known to increase the integrin‐mediated spreading of neutrophils derived from hematopoietic stem cells.39 Myeloid‐lineage specific Rac1 deletion reduces actin polymerization and the efficiency of chemotaxis,45 the latter by affecting directionality46 and uropod retraction.47 In vivo, conditional Rac1‐deficiency impairs neutrophil recruitment during sterile peritonitis45 and acute fMLP‐induced lung inflammation.48 Combined deficiency of Rac1 and Rac2 has more severe effects. This evidence concerns the gene RAC1 and inflammation.