These findings indicate that BD1-selective inhibition preferentially modulates cancer cell proliferation, while BD2 inhibition may more strongly regulate immuno-inflammatory responses, providing a rationale for indication-tailored BET targeting strategies in cancer and immune disorders [169].These findings indicate that BET inhibitors do not merely hold theoretical potential but have demonstrated preclinical efficacy in enhancing the effectiveness of immune checkpoint inhibitors, providing a strong rationale for translational development of such combinations in clinical settings. The gene discussed is DNER; the disease is cancer.