Specifically, the administration of dipeptidyl peptidase inhibitors has been reported to drive CXCL9 and CXCL10 secretion in experimental models of hepatocellular carcinoma (HCC) and pancreatic ductal adenocarcinoma (PDAC), culminating with CXCR3+ NK cell recruitment and (at least in some setting) synergy with immune checkpoint inhibitors (ICIs) [46, 47]. The gene discussed is CXCR3; the disease is hepatocellular carcinoma.