Another proposed IO combination of CXCR2 (receptor crucial to neutrophil recruitment and highly expressed in NASH-HCC) and anti-PD1 treatment aimed at inhibiting tumour-associated neutrophils demonstrated reprogramming of the tumour immune microenvironment that promotes ICI in NASH-HCC [109]. This evidence concerns the gene CXCR2 and metabolic dysfunction-associated steatohepatitis.