In Vitro: Induced apoptosis and ferroptosis by increasing ROS, upregulating PDL1 expression, and modulating ferroptosis-related proteins such as GPX4 and FTH1. In Vivo: Enhanced the anti-tumor efficacy of anti-PD1 immunotherapy by promoting PDL1 expression, increasing immune infiltration (CD4+ and CD8+ T cells), and inducing ferroptosis in a mouse model of NSCLC. The gene discussed is CD4; the disease is neoplasm.