The molecular mechanisms underlying the anti-tumor effects of combination blockade primarily include (1) triggering Fcγ receptor (FcγR)-dependent activation of tumor myeloid cells [28]; (2) eliciting the clonal expansion of tumor antigen-specific CD8+ T cells driven by CD226 [29, 32]; and (3) significantly upregulating pro-inflammatory cytokines in both CD4+ and CD8+ cells, including IL-2, IFN-γ, and TNF-α [33]. The gene discussed is CD4; the disease is neoplasm.