Specifically, genetic ablation of Stat3 in murine as well as STAT3 in human cells leads to an increase of NF-κB-induced expression of CXCL1/IL-8, which contributes to infiltration of myeloid cells as well as vascularization; while inhibiting CXCL1’s cognate receptor, CXCR2 can normalize tumor vascularization and microenvironment and reduce tumor burden [97]. The gene discussed is CXCL1; the disease is neoplasm.