Given the ability of PARP inhibitors to modify the tumor microenvironment, especially the recruitment and priming of CD4+ and CD8+T cells by producing neoantigen and releasing cytokines and chemokines, such as INF-γ, CCL5 and CXCL10 [10, 16], PD-1 inhibitors in combination with PARPi have potential to broaden durable responses and extend benefit populations of both PD-1 inhibitors and PARP inhibitors. The gene discussed is CD4; the disease is neoplasm.