Genetically engineered mouse models are genetically heterogeneous and therefore unlikely to manifest all of the potential mechanisms associated with resistance to PD-1 blockade and specifically are not suitable for the study of immune editing of specific tumour neoantigens or loss of antigen presentation as potential resistance mechanisms to anti-PD-1 therapy33, processes which will likely require evaluation in large cohorts of primary patient specimens. This evidence concerns the gene PDCD1 and neoplasm.