145). Mutations in the SWI/SNF complex, including ARID1A, contribute to resistance to immune checkpoint inhibitors, with ARID1A-deficient tumours showing better responses to anti-PD-L1 treatment. Inhibiting another SWI/SNF subunit, PBRM1, enhances immunotherapy responses by boosting tumour immunogenicity (Refs 146, 147). These findings suggest targeting the SWI/SNF complex may enhance the effects of immune checkpoint inhibitors in HCC, though more research is needed to understand the mechanisms involved (Ref. 148). This evidence concerns the gene SMARCA1 and neoplasm.