In recent years, due to an in‐depth understanding of the tumor immune microenvironment and the mechanism of tumor immune escape, treatment by targeted inhibition of immune checkpoint molecules such as programmed cell death‐1 (PD‐1)/programmed cell death ligand‐1 (PD‐L1) and cytotoxic T‐lymphocyte associated protein 4 (CTLA‐4) has brought a revolutionary change to the treatment of malignant tumors.1, 2. This evidence concerns the gene CTLA4 and neoplasm.