CHIP specifically impairs the formyl peptide response to reduce the production of chemotactic factors, thereby weakening neutrophil chemotaxis.21 FLIPr inhibits neutrophil chemotaxis by reducing intracellular calcium mobilization.22 Eap blocks neutrophil chemotaxis and recruitment by binding to intercellular adhesion molecule 1 (ICAM-1).23 These different virulence mechanisms make it difficult for neutrophils to rapidly chemotax and recruit to the infection site, significantly reducing the bactericidal effect of innate immunity. The gene discussed is ICAM1; the disease is infection.