This is followed by migration arrest at later stages of infection to avoid uncontrolled aggregation at inflamed sites through G protein-coupled receptor kinase 2 (GRK2)-mediated G protein-coupled receptors (GPCR) desensitization, and prostaglandin E2 (PGE2) synthesis to promote anti-inflammatory programs for tissue repair (119, 120). The gene discussed is GRK2; the disease is infection.