Mechanistically, BCLAF1 competitively inhibits SPOP-mediated ubiquitination and degradation of PD-L1 to promote HCC progression and evasion of immune surveillance, and overexpression of BCLAF1 enhances the efficacy of ICB therapy treated with Atezolizumab (Fig. 8). This evidence concerns the gene SPOP and hepatocellular carcinoma.