Moreover, enhancement of NO during sepsis can trigger the activation of soluble guanylate cyclase (sGC), cyclic‐GMP formation and protein kinase G (PKG) phosphorylation, all of which induce the expression of GRK2 in neutrophils, and promote the internalization of CXCR2 59 (Fig. 2). This evidence concerns the gene GRK2 and Sepsis.