Varying responses to PD-1 blockade have previously been observed in the MC38 model and are, in part, explained by tumour-intrinsic resistance mechanism such as pro-tumour regulatory T cells and macrophages of the M2 phenotype [45, 46] as well as, for example, differences in the microbiome of the murine hosts under different agistment conditions [47]. This evidence concerns the gene PDCD1 and neoplasm.