Specifically, we found that genetic inhibition of ERAP1 combined with entinostat administration, is able to i) induce the expression of MHC class I and PD-L1 molecules, ii) modify the immunopeptidome, iii) increase the recruitment of activated T cells and NK cells into the tumor microenvironment (TME) and, correspondingly, iv) overcome tumor resistance to PD-1 blockade. This evidence concerns the gene CD274 and neoplasm.