While GRK2 signaling has previously been implicated in chemotaxis of immune cells, in extravascular neutrophils GRK2-mediated arrest limits dynamic aggregation and thus the progression of cluster formation, which may be important in limiting collateral tissue damage and pathological inflammation in response to sterile disruptions.3 However, in the case of bacterial infection, this arrest is of even greater functional significance. This evidence concerns the gene GRK2 and bacterial infectious disease.