For example, rs11064 in TNFAIP8 could function by affecting the affinity of miR-22 binding to the 3′-UTR of TNFAIP8 and regulating TNFAIP8 expression, thus contributing to cervical cancer risk [14]; CXCR2 rs1126579 disrupted a novel binding site for miR-516a-3p, led to a moderate increase in CXCR2 mRNA and protein expression, and intensified MAPK signaling which reduced the risk of lung cancer [15]. This evidence concerns the gene CXCR2 and lung carcinoma.