CXCR2 and neoplasm: Interestingly, however, we have demonstrated that the pharmacological inhibition of both CXCR2 and PD-1 sensitises immunotherapy-resistant non-alcoholic steatohepatitis-associated HCC (NASH-HCC) mouse models to immune checkpoint blockade, resulting in an influx of intratumoural neutrophils that promote CD8+ T cell and CD103+XCR1+ cDC1 dendritic cell activation, leading to a decrease in tumour burden (Figure 5) [39].