While future research is necessary, D2R agonist treatment likely helps reprogramme the immunosuppressive tumour microenvironment to enhance immune responses through reduction of tumour-infiltrating myeloid-derived suppressor cells and stimulation of T cells, making the tumour highly susceptible to enhanced anti-cancer responses through immune checkpoint inhibitors like anti-PD1/CTLA4. The gene discussed is CTLA4; the disease is cancer.