CTLA4 and neoplasm: The sensitivity to ICIs detected in dMMR/MSI-H and POLE mutated tumours relies on a common hypermutated phenotype that causes the consequent development of neoantigens boosting an immune-inflamed (or “hot”) microenvironment, where Cytotoxic T-lymphocytes (CTLs) activity against tumour cells is restrained by immune checkpoint, like PD1/PD-L1 and CTLA-4/B7 axes, and may be released by ICIs [17,18].