Our work therefore emphasises the strong potential for targeted therapeutic manipulation of the innate immune system in cancer, but also uncovers a previously unrecognised crosstalk between the C-X-C chemokine/CXCR2 and PD1/PDL1 signalling systems that may be exploited to improve immunotherapy responses not only in NASH-HCC but also in other types of cancer that exhibit immunotherapy resistance.54 55. This evidence concerns the gene CXCR2 and metabolic dysfunction-associated steatohepatitis.