Consistent with our data that miR-722 directly downregulates endogenous rac2 expression, defects in neutrophil motility (Fig. 3B) or their recruitment to tissue injury (Fig. 3C) or infection (Fig. 3D; Movie 3) resulting from miR-722 overexpression were all rescued by rac2 overexpression, pinpointing rac2 as a relevant miR-722 target in neutrophils. This evidence concerns the gene RAC2 and infection.