In a prostate cancer model, CXCL8 increases the expression of mRNA and protein levels of ACKR3 (103); IL-1β triggers ACKR3 expression in HUVEC cells (104); and other external factors such as lipopolysaccharides associate with ACKR3 upregulation in the pulmonary epithelium modulating microvascular permeability during acute pulmonary inflammation (105). This evidence concerns the gene ACKR3 and prostate carcinoma.