Due to the high expression levels of miR-K3 in KS lesions [41] and the crucial role that the miR-K3/GRK2/CXCR2/AKT axis might play in the KS pathogenesis [40], in this study, we have shown that, by targeting GRK2, miR-K3 not only facilitates KSHV latency, but also mediates KSHV-induced angiogenesis by activating the CXCR2/AKT pathway. The gene discussed is CXCR2; the disease is Kaposi's sarcoma.