In conclusion, we preliminarily propose the following hypothesis: S100A10 may activate the cPLA2 and 5-LOX-LOX axis, where signal activation initiates lipid metabolism reprogramming, upregulates LTB4 levels, thereby promoting CD8+ T cell exhaustion in HCC tissues, leading to immune escape of HCC cells, ultimately affecting the growth and migration of HCC cells (Fig. 8). Here, ALOX5 is linked to hepatocellular carcinoma.