After knockout, the expression of tumor immunosuppressor-related proteins (PD-L1 and CD47) and proliferation-related proteins (C-MYC and Cyclin D1) was significantly downregulated, which also reversed the immunosuppression induced by PD-L1 in the presence of IFN-γ. These findings provide a strong incentive for CRISPR/Cas9 to explore IFN, PI3K-Akt, and Wnt//β-catenin signaling pathways and strategies to enhance tumor immune invasion, as a means to increase tumor sensitivity to immune checkpoint blockade therapy. The gene discussed is CCND1; the disease is neoplasm.