About 85% of primary liver cancer is Hepatocellular Carcinoma (HCC), which has a 5-year survival rate below 20%. We recently reported that mRNA expression of the Dipeptidyl Peptidase 4 (DPP4) gene family is highly upregulated in human HCC tumours compared to non-diseased liver tissue, and is associated with poor survival in HCC patients [1]. Pan-DPP compounds, which inhibit all the DPP4 enzyme family, such as talabostat and ARI-4175, can mediate tumour regression by immune-mediated mechanisms [2] that are believed to include NLRP1 activation. NLRP1 activation is inhibited by DPP9 [3]. DPP4 dampens CXCR3 stimulation. This study demonstrated that the pan-DPP inhibitory compound ARI-4175 significantly reduced the number of macroscopic liver nodules in a mouse HCC model. ARI-4175 increased intrahepatic inflammatory cell infiltration, CD8+ T cell numbers and the concentration of activated caspase-1 in the HCC-bearing liver. Autophagy markers were unaffected. In summary, this study provides promising data on the efficacy of ARI-4175 in the treatment of early-stage HCC. Targeting the DPP4 family may be a novel and effective approach to promote anti-tumour immunity in HCC via caspase-1 activation [4].