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). The gene discussed is BCLAF1; the disease is hepatocellular carcinoma.