CTLA4 and neoplasm: In addition, 13–15% of sporadic colorectal cancers and 25–30% of sporadic endometrial cancers are defective for mismatch repair as a direct result of bi-allelic promoter hypermethylation of the MLH1 gene, and this is relevant as it alters the prognosis of these tumours and patients with metastatic dMMR cancers may become eligible for immunotherapy using highly effective immune check point blockade agents such as anti-PD-1 (Pembrolizumab) or anti-CTLA4 (Nivolumab) monoclonal antibodies [31,32,45,46].