MAF and neoplasm: Moreover, a study that recently examined the regulatory network involved in the control of T-cell exhaustion in tumors underlined that although MAF and PRDM1 are together involved in controlling several co-inhibitory receptors expression in T cells, both factors do not interact together and that PRDM1 function in tumor-infiltrating T cells is independent of MAF suggesting that both TFs may have a compensatory role (116) Indeed, regression of tumor was observed more significantly in MAF, PRDM1 double KO mice than in mice with a single gene deletion.