Therapies based on immune checkpoint inhibitors, mainly the cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed-death receptor 1 (PD-1), demonstrated significantly poorer response rates in gynecologic tumors [82,83] with the remarkable exception of PD-1 inhibitors for the treatment of microsatellite instability-high (MSI-High) or mismatch repair-deficient (dMMR) metastatic ECs [84]. This evidence concerns the gene CTLA4 and female reproductive system neoplasm.