Indeed, our findings need to be further explored in a larger dataset, but a working hypothesis could be that MSI tumors accompanied by systemic inflammation exhibit a highly myeloid immune infiltrated TME resulting in an immunosuppressive state either caused by 1) a compensatory upregulation of immune checkpoints stimulated by preexisting cytokines such as IFN-gamma following the MSI-induced active immune microenvironment leading to a functional exhaustion of the T cells or 2) direct immunosuppressive and tumor-promoting effects exerted by the myeloid cells themselves. This evidence concerns the gene IFNG and neoplasm.