Given that IGF1 could delay apoptosis of neutrophils while CXCL12/CXCR4 was key retention and migration signal for neutrophil activities [74, 75], fibroblast and macrophage cell circuits potentially exacerbate inappropriate retention and anti-apoptosis of neutrophils at inflammatory sites, acting as a major driver of the excessive damage characteristics in asthma. Here, CXCR4 is linked to asthma.