Finally, the data discussed in this review strongly imply that HMAs may have the potential to counteract factors that contribute to primary resistance to immune checkpoint blockade therapy, and thus may (re)sensitize tumors with (a) low numbers of tumor infiltrating T-cells, (b) low expression of the IFN-response gene expression signature, and/or (c) high expression levels of inhibitory immune checkpoint molecules to targeted immune checkpoint modulation. This evidence concerns the gene IFNA1 and neoplasm.