showed that, in an Rb1/Tp53-deficient, syngeneic and immunocompetent SCLC model, co-treatment with the LSD1 inhibitor bomedemstat and PD-1 blockade markedly expanded intratumoral CD8+ T cells and produced robust tumor growth inhibition—findings that now underpin a planned clinical trial combining bomedemstat with standard PD-1 axis therapy in SCLC (177). The gene discussed is CD8A; the disease is neoplasm.