Tumor cells evade immune surveillance by upregulating immune checkpoints, contributing to progression and immunotherapy resistance.40,41 YAP has been implicated in PD-L1 regulation across multiple cancers, where its activation enhances PD-L1 expression and suppresses T-cell function.25,42 In this study, we identified dysadherin as an upstream activator of the YAP–TEAD2 complex in HCC that directly drives PD-L1 transcription and impairs cytotoxic T-cell activity in a humanized HCC model. The gene discussed is TEAD2; the disease is cancer.