Huang X et al. showed for the first time that FOXM1 is the critical downstream target of endothelial p110γ and indicated that CXCL12 signaling-activated p110γ (GPCR-dependent p110γPI3K) in endothelial cells mediates FOXM1 upregulation, thereby promoting endothelial regeneration and vascular repair after inflammatory injury induced by endotoxemia and polymicrobial sepsis [84]. The gene discussed is FOXM1; the disease is serum lipopolysaccharide activity.