PRDM1 overexpression in hepatocellular carcinoma has been described as promoting PD-L1 expression via the USP22-SPI1 pathway, leading to CD8+ T cell exhaustion and immune evasion, while combination treatment with PD-1 blockade enhances anti-tumor immunity, suggesting a novel therapeutic strategy for HCC [68]. The gene discussed is SPI1; the disease is neoplasm.