Studies showed that CXCR3+ NK cells infiltrate tumors in a CXCL10-dependent fashion, leading to improved survival,196 while NK cells from CXCR3−/− mice show impaired tumor infiltration.309 Similarly, inhibiting pro-tumorigenic chemokine signaling enhances the potential of anti-tumorigenic chemokines, as exemplified by the knockdown of transcription factor Snail, reducing the expression of CXCR2 ligands (CXCL1 and CXCL2), and MDSCs attraction to the tumor via CXCR2, leading to increased T-cell and NK cell numbers in tumors.310. The gene discussed is CXCL10; the disease is neoplasm.