CXCR3 and neoplasm: They propose that Dipeptidyl peptidase (DPP4) inhibition increases tumor content of CXCL9/10, which recruits CXCR3 + NK and T cells, and DPP8/9 inhibition activates the inflammasome, resulting in proinflammatory cytokine release and Th1 response, further enhancing the CXCL9/10-­CXCR3 axis.